ENDOCRINOLOGY &

REPRODUCTION MODULE
(INTEGRATED TUTORIAL)
COLLEGE OF MEDICINE- THRID YEAR -2nd SEMESTER

2023-2024
IMAM ABDULRAHMAN BIN FAISAL UNIVERSITY –COLLEGE OF MEDICINE
Instructions:
• As we are introducing integrated questions in the Exams, so these integrated tutorials are
designed to orient the students for integrated teaching and learning.
• This tutorial summarizes most of the concepts delivered in the 4 weeks of the
Endocrinology & Reproduction module in 2nd semester in MED301 in an integrated
manner.
• Kindly have a detailed study of the given cases and the related triggering questions. So
that you should be fully prepared for the tutorial.

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 Case I: Type 2 Diabetes Mellitus
Learning Objectives: Student will be able to

Anatomy:
• identify location and recognize important anatomical relation of pancreas (taught in
GIT Module)
• Identify parts of pancreas and main and accessory pancreatic ducts. (taught in GIT
Module)
• Identify the blood and nerve supply of pancreas. (taught in GIT Module)
• Discuss histology of pancreases especially the endocrine part. (taught in GIT Module)

Physiology:
• Discuss the endocrine cell types of the pancreas and the respective hormones secreted
by them.
• Explain the mechanisms of Insulin and Glucagon release from the pancreatic cells.
• Discuss the mechanism by which insulin reduces blood glucose levels.
• Describe the actions of Insulin and Glucagon.
• Discuss the consequences and complications of Insulin resistance.
• Describe the physiological basis of diabetes and its symptoms.
• Understand physiological differences between type 1 and type 2 diabetes.
• Concept of insulin resistance in relation to obesity and metabolic syndrome.

Biochemistry: NA

Pharmacology:
• Differentiate between type 1 & type 2 diabetes mellitus
• Describe the complications associated with diabetes
• Describe the roles of insulin (and glucagon) in the control of blood glucose levels
• List the different formulations of insulin
• Discuss the types, mechanism of actions, uses, adverse reactions,
contraindications, precautions, and interactions of the antidiabetic drugs

Microbiology: NA

Clinical Skills:
• To practice and integrate elements of multiple systems to take a history from a person
with diabetes
• Discuss common symptoms and signs of diabetes and related complications
• Examination of the lower limbs and observing the complications of diabetes
• Demonstrate and discuss use of a glucometer.

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 Case Scenario+ questions: Type 2 Diabetes Mellitus
A 45-year-old software engineer Hamza who is working as a consultant in a reputed IT company
sought an appointment with his primary care physician (PCP) because he had felt increasingly
tired over the last few weeks, and it was starting to affect his work. He also complained of
feeling thirsty and of going to the washroom frequently to urinate, especially during the night,
which was unusual for him. His late mother had a history of type 2 diabetes.

He admitted to smoking 20–30 cigarettes per day, and consuming carbonated soft drinks while
having food, eating lots of high caloric foods such as pizza, burgers, and sweets. He is so
involved in his recent projects on artificial intelligence that he does not find enough time to do
exercise and eat food at home.

He rarely came to see the PCP. His previous medical history was osteoarthritis of the knee, for
which he is taking diclofenac 50 mg orally three times daily after food and omeprazole 20 mg
orally daily for gastroprotection.

On examination the vital signs showing a pulse 90 beats per minute, respiratory rate 20 breaths
per minute, temperature 37 C, blood pressure 158/90 mm Hg (reference range 120/80 mm Hg) in
sitting position and 164/90 mm Hg in standing position.

He is obese with a body mass index 32 kg/m2 (reference range 18.5 – 25 kg/m2) and a waist
circumference 124 cm (<94cm). Xanthelasmas are present in the bilateral periorbital areas.

Systemic examination is unremarkable.

On the initial lab investigations, urine dipstick test is positive for glucose, traces of protein but
not ketone bodies. His random blood glucose is 250 mg/dL.

The doctor asked the patient to come back for certain laboratory tests the next morning.
On examination his BP 160/90 mm Hg. General condition is stable and systemic examination
unremarkable.

His lab results are as follows:

• Fasting blood glucose 160 mg/dL (reference range 70-100 mg/dL)

• HbA1c 8.0% (normal <6%)
• Total cholesterol 280 mg/dL (reference range 150-199 mg/dL)
• LDL cholesterol 140 mg/dL (normal <100 mg/dL)
• Triglycerides 250 mg/dL (reference range 150-199 mg/dL)
• Blood urea 20 mg/dL (reference range 8-20 mg/dL)
• Serum creatinine 0.9 mg/dL (reference range 0.7-1.2 mg/dL)

The doctor diagnosed type 2 diabetes mellitus with dyslipidemia. He prescribes metformin 500
mg twice daily, simvastatin 10 mg once daily in the evening and multivitamins once daily. The
patient is also explained about the side effects of the prescribed medications.

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He also advised him to reduce his body weight by adopting healthy lifestyles such as eating a
healthy diet, avoiding alcohol and smoking, to do regular moderate exercise and how to take care
of his feet.

An appointment for the next follow up is given. He is also referred to a physician for the cardiac
evaluation and an ophthalmologist for the funduscopic examination.

After 3 months the patient came back for the follow up. He continued to have mild tiredness with
less frequent nocturnal polyuria. Cardiac evaluation and fundoscopic examination are found to
be normal.

The follow-up lab test results show

o Fasting blood glucose 145 mg/dL
o HbA1c 7.5%
o LDL cholesterol 110 mg/dL,
o Renal function tests are within the normal range

The doctor added tablet glimepiride 1 mg once daily along with metformin. The patient is also
explained about the side effects of glimepiride and what precautions should be taken if he
experiences signs and symptoms of hypoglycemia.

An appointment for the next follow-up given.

Anatomy:

Q1. The patient is diagnosed to have type II diabetes mellitus. Resistance to insulin is
described as the cause for this disease. Which cell type produces insulin in the body? And
in which organ is this cell type present?

Beta cells in the pancreas produce insulin in the body.

Q2. Give a brief histological description for this cell type.

Beta cells have a characteristic granular cytoplasm due to numerous insulin granules. They are
typically arranged in clusters within the islets and have a well-developed endoplasmic reticulum
to support their high rate of protein synthesis. Additionally, beta cells have a relatively large
nucleus with prominent nucleoli.

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Q3. Describe the mode of secretion of insulin and how it reaches the tissues.

Insulin is secreted by the beta cells of the pancreas in response to elevated blood glucose levels.
When we consume food, particularly carbohydrates, the glucose levels in our blood increase.
This triggers the beta cells to release insulin into the bloodstream.
Insulin then travels through the bloodstream to various tissues in the body, including muscle, fat,
and liver cells. Insulin acts as a key, allowing glucose from the bloodstream to enter these tissues
and be used for energy production or stored for later use.

Q4. Mention 2 arteries that supply this organ where insulin-secreting cells reside.

1. Pancreaticoduodenal arteries 2. Splenic artery

Q5. How is this organ related to the peritoneum? Mention its anterior & posterior
relations.

Anterior relations: Stomach, Greater omentum, transverse colon, and transverse mesocolon.
Posterior relations: Aorta, Superior Mesenteric Artery (SMA), Left suprarenal gland, Left kidney,
and Renal vessels.

Q6. What are the Islets of Langerhans and where are they located?

The Islets of Langerhans are groups of cells in the pancreas that produce and secrete hormones.
These cells regulate blood sugar levels by producing insulin and glucagon. The Islets of
Langerhans are located throughout the pancreas, scattered among the pancreatic tissue.
(Abundant in the tail of the pancreas)

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Q7. What happens to the Islets of Langerhans in individuals with type 1 and 2 diabetes?

• In type 1 diabetes (Loss of islets): The Islets of Langerhans in the pancreas are destroyed
by the immune system, leading to a decrease in or complete absence of insulin
production. This results in high levels of glucose in the blood, as insulin is necessary for
the body to properly regulate blood sugar levels.
• In type 2 diabetes (Insulin resistance) the Islets of Langerhans may initially produce
normal or
even increased levels of insulin in response to high blood sugar levels. However, over time, the
cells in the Islets may become resistant to the effects of insulin, leading to reduced insulin
production or decreased sensitivity to insulin. This can also result in high blood sugar levels and
the development of diabetes.

Physiology:

Q8. Hamza’s presenting complaints are polyuria, polydipsia and nocturia. Name the
diseases that can cause polyuria, polydipsia & nocturia?
Diabetes Insipidus (central/nephrogenic), Diabetes Mellitus (Type 1 & 2).
Q9. How you can differentiate between polyuria, polydipsia & nocturia caused by Diabetes
Mellitus or Diabetes Insipidus in following lab investigations?
Parameters Diabetes Mellitus (Type 1 Diabetes Insipidus (Central
or 2) or nephrogenic)
Fasting blood sugar Elevated Normal
Serum Insulin Low (Type1), normal or high Normal
(Type 2)
Serum ADH High (due to increase plasma Low (central), normal or
osmolarity) high (nephrogenic)
Urine glucose Positive negative
Urine osmolarity High (due to the presence of Low
glucose in urine)
Plasma osmolarity High (due to hyperglycemia) High

Q10. What are the risk factors of Diabetes Mellitus Type 2 in Hamza (modifiable and non-
modifiable)?
Modifiable Risk Factors: smoking, unhealthy eating style, sedentary lifestyle, obesity,
dyslipidemia
Non-modifiable: Family history of diabetes.

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Q11. Why Urinary ketone bodies are negative in T2DM (as in Hamza) but positive in
T1DM?

Severe Insulin deficiency in T1DM leads to an excess of counter-regulatory hormones

(glucagon, cortisol, epinephrine, growth hormone). This leads to hyperglycemia and excessive
fat breakdown resulting in increased ketone body production.
In T2DM, insulin levels are either normal or elevated. Hence ketone body production is limited.

Q12. What other endocrine disorders can produce hyperglycemia?

Acromegaly, Gigantism, Cushing’s Syndrome, Pheochromocytoma

Q13. Dr warns Hamza that uncontrolled Diabetes may make his vision blurry and can
cause kidney failure. What is the physiological mechanism behind diabetes-induced blurry
vision and kidney failure?

Uncontrolled diabetes may affect small blood vessels supplying retina and kidneys. This leads to
microvascular retinopathy that cause blurry vision and microvascualr nephropathy that cause
renal failure. Also, glucose accumulates in the eye as retina is an insulin-independent tissue.
Enzyme aldol reductase converts excess of glucose to Sorbitol, an osmotically active substance.
The presence of glucose, sorbitol etc. increases osmotic pressure inside the eye, drawing water
inside resulting in swelling of the lens. This changes the focal length of the eyes....blurry vision.

Q14. What is HbA1C and what is its significance in Diabetes Management?

It's like an average of your blood glucose over the past 2 or 3 months; it's used not only to
diagnose diabetes but also to monitor how well your diabetes treatment is working overtime.

Biochemistry: NA

Pharmacology:
Q15. What are the early adverse effects of metformin?
GIT upset including nausea, diarrhea & abdominal pain

Q16. How can we prevent these early adverse effects associated with metformin?
These early adverse effects can be reduced with meal consumption and by gradually increasing
the dose of metformin

Q17. What is the mechanism of action in which glimepiride can lower blood glucose levels?
It binds to and blocks the activation of ATP-sensitive K+ channels (KATP channels) on the
plasma membrane of the pancreatic β-cells leading to depolarization of the cells, increased influx
of Ca2+ and enhancement of the secretion of insulin.

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Q18. What is the effect of chronic use of glimepiride on the pancreatic β-cells?
Chronic use of glimepiride can accelerate pancreatic β-cells exhaustion & apoptosis

Microbiology: NA

Clinical Skills:
Extended stem: Patient also complained of excessive sweating, blurry vision, headache and
recent history of occasional tingling sensation in the legs.

Q19. What are the symptoms of hypoglycemia which Hamza should be conscious of?
sweating, anxiousness, morning headaches, dizziness, extreme tiredness, and blurred vision
Q20. Name the endocrine disorders which can cause type 2 diabetes mellitus?
Cushing’s syndrome, acromegaly, glucagonoma, pheochromocytoma
Q21. List the modifiable and non-modifiable risk factors in Hamza?
modifiable:
obesity, physical inactivity, stress, unhealthy diet, smoking, alcohol intake.
non - modifiable:
age- 45 years, family history
Q22. Which are the major risk factors in Hamza for developing cardiovascular disease?
Diabetes mellitus with obesity
Q23. Which is the test for checking mean plasma glucose concentration over the previous
8-12 weeks?
a) Hemoglobin A1c (Answer)
b) Oral glucose tolerance test (OGTT)
c) Fructosamine test
d) Fasting plasma glucose concentration
Q24. Which statement is correct regarding newly diagnosed type 2 diabetes patient?
a. Insulin is not used to control blood glucose in patients with type 2 diabetes.
b. Complications of type 2 diabetes are less serious than those of type 1 diabetes.
c. Changes in diet and exercise may control blood glucose levels in type 2 diabetes. (Answer)

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d. Type 2 diabetes is usually diagnosed when the patient is admitted with a
hyperglycemic coma.
Q25. What is the beneficial effect of exercise on diabetes in Hamza?
Increase in insulin sensitivity
Q26. In addition to diet, exercise, and smoking cessation, which of the following would have
the largest impact in reducing Hamza’s cholesterol?
a. Controlling his blood pressure
b. Decrease alcohol consumption
c. Improving his sleeping habits
d. Controlling his diabetes (Answer)
Q27. Why is it essential for Hmaza to examine his feet regularly?
To avert the complications of peripheral neuropathy like leg ulcers

Reading Material Case I: Type 2 Diabetes Mellitus

Anatomy:
• Gray’s Anatomy for students
• Clinical Anatomy for medical students (Richard Snell)

Physiology:
• Human Physiology by Lauralee Sherwood (9th Edition) [Pages 693-701]
• Lecture slides

Pharmacology:
• Lecture slides

Clinical Skills:

• [Link] NJ & O'Connor S Clinical Examination: A systematic guide to physical

diagnosis 8th ed CHAPTER 27 The endocrine history (p:438-443), CHAPTER 29
Correlation of physical signs and endocrine disease (p:463-469) and CHAPTER 30 A
summary of the endocrine examination and extending the endocrine examination (p:481
& 483)
• Diagnosis and classification of Diabetes mellitus:
[Link]

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 Case II: Addison’s disease

Learning Objectives: Student will be able to

Anatomy:
• Describe the location, structure, and relation of right and left adrenal glands.
• Discuss the blood supply (differences)of right and left adrenal glands.
• Describe the relation of renal fascia to the adrenal glands.
• Discuss the histology of adrenal glands.

Physiology:
• Discuss the actions of hormones from adrenal cortex.
• Discuss the factors regulating the secretion of adrenal cortical hormones.
• Describe the diurnal variations in plasma cortisol levels and explain their clinical
significance.
• Describe the role of hypothalamic pituitary adrenal axis in controlling levels of
hormones from adrenal cortex.
• Describe common presenting signs/symptoms of under-secretion of hormones from
adrenal cortex.
• Discuss the ways in which these signs/symptoms relate to our understanding of adrenal
physiology.

Biochemistry: NA

Pharmacology: NA

Microbiology: NA

Clinical Skills:
• Take focused medical history of the endocrine system
• Demonstrate some endocrine physical examination skills, for examining common
endocrine conditions.
• Selection of investigations and imaging techniques used in the diagnosis and
management of patients presenting with endocrine abnormalities.

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 Case Scenario+ questions: Addison’s disease
Mrs. Jamila, a 32-year-old, high school teacher presented to the outpatient department with 2-
year history of increasing darkening of the skin, dizziness, and easy fatigability.
She also complained of nausea with occasional vomiting, progressive weight loss of about 10
kgs over past eight months prior to presentation. Furthermore, patient reported decreased
appetite, salt craving, excessive sweating, disturbed sleep habits and mood changes
There was no history of headache, blurred vision, and neither loss of consciousness nor change
in her bowel habit. The systemic review revealed no abnormality.
No history of tuberculosis, diabetes mellitus or thyroid disorder. The patient’s mother has
rheumatoid arthritis , father died of cardiac condition and sister with Hashimoto thyroiditis .
She had irregular menstrual history and decreased sexual drive.

Physical examination findings:

On general physical examination, the patient was thin built, appeared weak with generalized
hyperpigmentation especially on the face, oral mucosa, palmar creases, and knuckles. Loss
of axillary and pubic hair were also noted. There was no significant peripheral
lymphadenopathy.
Main findings in the systemic examination were a pulse rate of 116 bpm, regular, low volume,
thread pulse without any radio radial or radio femoral delay and blood pressure of 90/60
mmHg in supine position. The remaining physical examination of the cardiovascular,
respiratory and abdominal systems were unremarkable.

Laboratory findings:
Blood tests showed hyponatremia with sodium at 128 mmol/L (reference range 135–145
mmol/L), potassium at 5.4 mmol/L (reference range 3.5–5.2 mmol/L), elevated urea at 8.9
mmol/L (reference range 2.9–7.7 mmol/L), and serum creatinine was 0.9 mg/dl (0.6-1.4). C
reactive protein (CRP) was elevated at 24 mg/L (reference range 0–8 mg/L)
Early morning 8 am serum cortisol levels were low 0.59 µg/dl (6.20-14.9 µg/dl). Serum
aldosterone level was in the lower range of 1.7 (1-16) measured at rest. Plasma ACTH levels
were significantly raised >1250 pg/ml (normal is (normal is < 46 pg/ml).

In view of above findings, she was diagnosed as a case of primary adrenal insufficiency -
Addison’s disease.

She was treated with hydrocortisone 10-5-5 mg, Tab Fludrocortisone 0.1 mg OD. and started
feeling better with significant improvement of the symptoms after few weeks of treatment.

Anatomy:

CT scan adrenal revealed bilateral adrenal hyperplasia with calcification.

Q1. Mention the parts of the adrenal gland and which of these parts is affected in
Addison’s disease.

Histologically adrenal gland has a cortex and medulla. The cortex is affected by Addison's
disease.

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Q2. Describe the blood supply of the adrenal glands.

The arterial supply to the suprarenal glands is extensive and arises from three primary sources
1. Superior suprarenal arteries: A branch of an inferior phrenic artery
2. Middle suprarenal arteries: Usually arise directly from the abdominal aorta.
3. Inferior suprarenal arteries: From the renal arteries.
In contrast to this multiple arterial supply is the venous drainage, which usually consists of a
single vein leaving the hilum of each gland. On the right side, the right suprarenal vein is short
and almost immediately enters the inferior vena cava, while on the left side, the left suprarenal
vein enters the left renal vein.

Q3. What are the relations of this gland on both sides?

Anterior relation: the right suprarenal gland is related to the right lobe of the liver and the
inferior vena cava, and the left suprarenal gland is related to the part of the stomach, pancreas,
and, on occasion, the spleen.
Posterior relation: both the glands are related to the diaphragm.

Q4. What are the three layers of the adrenal cortex, and what hormones do they
produce?

Cortex has three-zone

1. Zona glomerulosa: Mineralocorticoid (aldosterone)
2. Zona fasciculata: Glucocorticoids
3. Zona reticularis: Androgen

Q5. Which layer of the adrenal cortex is primarily affected in the given case?

Zona fasciculata

Q6. How is Addison's disease diagnosed histologically?

Addison disease or adrenal cortical insufficiency is a disorder, usually autoimmune in origin,

which causes degeneration in any layer of the adrenal cortex, with concomitant loss of
glucocorticoids, mineralocorticoids, or androgen production.

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Physiology:

Q7. What are the underlying physiological mechanisms for following symptoms in
Jamila?

• Hyperpigmentation:
Low cortisol results in increased ACTH production and secretion. ACTH and MSH are
produced from a common precursor. Hence, increased production of ACTH results in
concurrent increased production of MSH. In addition, ACTH resembles closely to MSH and
when ACTH levels are high, some of it binds with MSH receptor as well, resulting in more
melanin secretion.
Hyperpigmentation is more pronounced over palmar creases, gingival mucosa, lips, elbows,
knuckles, posterior neck, and nail beds.
• Salt craving:
Salt craving is due to hyponatremia. Lack of aldosterone caused salt and water loss through
urine. Low ECF volume and low BP stimulates ADH secretion which worsens hyponatremia.
• Dizziness:
Lack of cortisol causes hypoglycemia and postural hypotension. This leads to dizziness.
Q8. What are the underlying physiological mechanisms for hyponatremia and
hyperkalemia in Jamila?
Hyponatremia and hyperkalemia are due to lack of Aldosterone. Hyponatremia is also due to
the increased release of antidiuretic hormone (ADH) in response to decreased sodium and
decreased BP/Blood volume.
Q9. What change is expected in plasma Renin levels of Jamila and why?
A: Jamila is having Primary adrenocortical insufficiency. Low aldosterone will lead to high
plasma Renin.
Q10. Differentiate between Primary, secondary and tertiary adrenocortical insufficiency.
Addison’s disease belongs to which of these categories?
Answer: Addison's disease is Primary adrenocortical insufficiency/

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Q11. Name all layers of adrenal gland and list their hormones.
Zona Glomerulosa: Aldosterone
Zona Fasciculata: Cortisol
Zona Reticularis: Sex steroids (Dehydroepiandrostenedione)
Q12. Comment on the levels of Aldosterone in Primary, secondary and tertiary adrenal
insufficiency.
Aldosterone levels are low in Primary Adrenocortical insufficiency, whereas aldosterone levels
are normal/minimal affected in Secondary and Tertiary adrenocortical insufficiency.
Q13. What is the underlying mechanism of high urea level in Jamila?
High Urea or blood urea nitrogen (BUN) could be due to the hypovolemia/severe dehydration,
a decreased glomerular filtration rate, and a decreased renal plasma flow.
Q14. Comment on adrenal medulla size and its hormones in Jamila?
Jamila is having Addison’s disease which affects adrenal cortex and its hormones only.
Adrenal medulla and its hormones are spared.
Biochemistry: NA

Pharmacology: NA

Microbiology: NA

Clinical Skills:
Extended stem:

She was given a follow-up appointment for the potential adverse effects (if any) and to recheck
her blood pressure. 3 months later she presented to the family health center complaining of a
new onset of headache, sometimes migraine and weight gain. Physical examination revealed:
BP was 160/90, BMI was 29 and others were insignificant.

Q15. What is the most common cause of Addison’s disease globally?

Autoimmune disease of the adrenal glands.
Q16. What are the other clinical features of Addison’s disease?
Postural hypotension, profound dehydration, shock, acute abdominal pain, unexplained fever,
Vitiligo.

Reading Material Case II: Addison’s disease

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 • Anatomy: Gray’s Anatomy for students
• Clinical Anatomy for medical students (Richard Snell)

Physiology:
• Human Physiology by Lauralee Sherwood (9th Edition) [Pages 672-682]

Clinical Skills:
[Link] NJ & O'Connor S Clinical Examination: A systematic guide to physical diagnosis 8 th
ed CHAPTER 28 The endocrine examination
2. Epstein O, Perkin GD, de Bono DP & Cookson J 2008 Clinical Examination 4th ed
CHAPTER 2 The general examination

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 Case III: Contraception
Learning Objectives: Student will be able to

Anatomy:
Clinical anatomy of the uterus and other parts of female reproductive system

Physiology:
• Identify the ovulation and the fertile window
• Determine the methods to identify the fertile window
• Discuss the various contraceptive methods and the underlined mechanisms

Biochemistry: NA

Pharmacology:
• Outline the role of hypothalamus-pituitary-gonadal axes and its feedback
• Discuss the mechanism of action, uses, adverse effects, contraindications,
precautions, and interactions of the hormonal contraceptives

Microbiology: NA

Clinical Skills:
• To take a focused history of a sexual and reproductive health problem
• To recognize the common risk factors for a sexual and reproductive health problem
• To recognize the role, contraindication and effectiveness of various contraceptive
methods

Case Scenario+ questions: Contraception

A healthy 25-year-old female Filipino who is married, presents to family health center for a
routine well woman examination. She is a gravida-2, para-2, with 2 living children.
She is visiting the health center today to be evaluated for the use of hormonal contraceptives to
prevent an unwanted pregnancy. She desires to conceive again but not soon. The patient states
she has heard about various contraceptive options, and she wants to know more about those
options, and if they would be okay for her to try.

She denies any prior sexually transmitted infections. She is a non-smoker, non-alcoholic and
she denies the use of illicit or recreational drugs. Past medical history is insignificant.

The patient states she attained menarche at age 14, with irregular cycles of 25–36 days in
duration. Her last menstrual period was two weeks ago.

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Physical examination:

General: Well-developed and well-nourished female

Vital Signs: Pulse 80 bpm, BP 120/80 mm Hg, Temp 37°C; weight 56 kg, height 5’6”
Skin: Mild facial acne
Neck/Lymph Nodes: Supple without lymphadenopathy or thyromegaly
Breasts: Equal in size without nodularity or masses, non-tender
Abdomen: Soft, nontender, no masses or organomegaly
Pelvic: Normal vaginal exam without tenderness or masses
CVS/RS/Neurological; unremarkable
Lab results: Negative Pap smear and urine pregnancy test.

She was prescribed combined oral contraceptive pills for two years. The doctor explained how
and when to take the pills, the short-term and long-term adverse effects of the prescribed pills.
She was given a follow-up appointment for the potential adverse effects (if any) and to recheck
her blood pressure.

Anatomy:

Her friend advised her to use a contraceptive device which can be inserted by doctor in her
reproductive organ in a minor OT procedure. She has read on the internet that it is safe and
long acting.

Q1. What are the non-surgical, effective contraception options?

There are several highly effective contraception options other than surgeries.
1. Natural family planning: Tracking menstrual cycles and avoiding sex during fertile
periods.
2. Barrier methods: These include male and female condoms, diaphragms, and cervical
caps. They physically block sperm from entering the uterus.
3. Birth control pills: Oral contraceptives that contain hormones to prevent ovulation and
thicken cervical mucus, making it difficult for sperm to reach the egg.
4. Contraceptive patches: Thin, adhesive patches that release hormones into the
bloodstream to prevent pregnancy. They are usually placed on the skin once a week.
5. Intrauterine devices (IUDs): Small, T-shaped devices inserted into the uterus to prevent
pregnancy. There are hormonal and non-hormonal IUD options available.
6. Contraceptive injections: Hormonal injections are administered every few days of
months to prevent ovulation and thin the uterine lining.

Q2. What are the new minor invasive methods, that are effective contraceptive options
with good reversal rates after removal?

Contraceptive implants: Small, flexible rods inserted under the skin that release hormones to
prevent pregnancy. They are effective for several years.

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Physiology:
The patient states she has heard about various contraceptive options including the natural
contraception method, and she wants to know more about those options, and if they would be
okay for her to try.

Q3. If the female has a regular cycle, when is the fertile window and how she can
determine the fertile period?

In regular 28-day cycle, OVULATION will be at 14 days from the 1st day of bleeding.
Fertilization must occur within 24 hrs. after ovulation when the ovum is still viable.

Calendar method, Temperature method, cervical changes, hormonal changes.

Q4. To explain the natural contraception method, which event of the fertilization process
can be prevented?

Blocking sperm transport to the ovum.

Q5. To help the patient to decide about the most effective way of contraception, order the
failure rate of the following methods (from low to high failure rate):

Intrauterine device, Barrier method, Natural method, Implanted contraceptives, Oral

contraceptives.

Implanted contraceptives, Oral contraceptives, Intrauterine device, Barrier method, Natural

method.

Biochemistry: NA

Pharmacology:

She was prescribed combined oral contraceptive pills for two years. The doctor explained how
and when to take the pills, the short-term and long-term adverse effects of the prescribed pills.
She was given a follow-up appointment for the potential adverse effects (if any) and to recheck
her blood pressure.

Q6. What are the indications of hormonal contraceptive pills?

1. To prevent pregnancies that are too early, too frequent and too many
2. To reduce the infant and maternal mortality rate

Q7. Write the mechanism of action of combined oral contraceptive pill?

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They prevent ovulation by negative feedback on hypothalamus

Estrogen inhibits secretion of FSH thus suppresses development of the ovarian follicle

Progestin ↓ GnRH release and thus ↓midcycle LH

Progestin also contributes to the contraceptive effects by

➢ Thickening of cervical mucus (↓ penetration by sperms)

➢ Impairing the tubal motility & peristalsis
➢ ↓likelihood of implantation

Q8. List non-contraceptive uses of oral contraceptive pills.

Ovarian cysts, Primary hypogonadism, Acne & hirsutism, Endometriosis

Menstrual cycle disorders:

➢ Polycystic ovary syndrome

➢ Abnormal uterine bleeding
➢ Premenstrual dysphoric disorder/dysmenorrhea

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Q9. Give reasons why the OCPs should not be taken while on drugs like rifampicin,
phenytoin, carbamazepine, and St. John’s wort?

The co-administered drugs induce the hepatic CYP 450 enzymes thereby decreasing the serum
estrogen & progestin levels thus causing contraceptive failure.

Microbiology: NA

Clinical Skills:
She was given a follow-up appointment for the potential adverse effects (if any) and to recheck
her blood pressure. 3 months later she presents to the family health center complaining of a
new onset of headache, sometimes migraine and weight gain. Physical examination revealed:
BP was 160/90, BMI was 29 and others were insignificant.

Q10. What are the contraindications for combined oral contraceptive pills?
Not to be used in breastfeeding women. Won’t protect from STIs. Not good if have – certain
types of migraine, are very overweight, have HTN, heart or liver conditions, are a smoker (esp
if over 35yo), are on certain medications

Q11. What is the most suitable hormonal contraception for lactating women?
Progesterone Only Pill (POP, Mini Pill)

Q12. What is the mechanism of action of combined oral contraceptive pills?

Thickens cervical mucus, may stop ovulation each month, may stop uterine implantation.

Q13. Emergency contraception is most effective when taken within how many hours
after unprotected intercourse?
1. 12 hours
2. 24 hours
3. 72 hours (Answer)
4. 120 hours

Q14. What are the common side effects of combined oral contraceptive pills?
May feel sick, may bleed between periods, or have sore breasts, headaches, bloating, mood
swings or changes to your skin.

Reading Material Case III: Contraception

Anatomy:
• Gray’s Anatomy for students
• Clinical Anatomy for medical students (Richard Snell)

Physiology:
• Sherwood, Human Physiology from cell to system, (9th edition, Ch. 20, page 753, 758-
759 and Lecture 5, Fertilization and early embryonic life)

20
Pharmacology:
• Basic & Clinical Pharmacology by BG Katzung 15e, Ch 40
• Goodman & Gillman’s pharmacological basis of therapeutics 14e Ch 44
• [Link]

Clinical Skills:
• Talley NJ & O'Connor S Clinical Examination: A systematic guide to physical
diagnosis 8th ed
• [Link] (follow the link to information
on various contraceptive forms)

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 Case IV: Sexually Transmitted Diseases (STD)
Learning Objectives: Student will be able to

Anatomy:
• Describe the gross anatomy of the penis, and its blood supply, nerve supply, and
lymphatic drainage.
• Describe the gross anatomy of the Vulva and vagina, and its blood supply, nerve supply,
and lymphatic drainage.

Physiology: NA

Biochemistry: NA

Pharmacology:
• To know the common STDs.
• To know the mechanism of action, adverse effects and contraindications of the drugs
used to eradicate STDs.

Microbiology/parasitology:
• Various microbes transmitted sexually
• Virulence factors and pathogenesis of STDs
• Primary signs & symptoms of STDs
• Various diagnostic methods available to diagnose STDs
• Various methods of management of STDs
• profound impact on sexual and reproductive health
• various stigma attached to STDs and the role it plays
• importance of prevention and control of STDs

Clinical Skills:
• To take a focused history of a sexual and reproductive health problem
• To recognize the common risk factors for a sexual and reproductive health problem
• To recognize the common presentation for a particular condition
• To use clinical reasoning in deciding what investigation may be required to aid in
diagnosis and management

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 Case Scenario+ questions: Sexually Transmitted Diseases (STD)

A 28-year-old university drop out man working as truck driver living in a metro city in
America came to the Genito urinary disease clinic with a chief complaint of a sore on his shaft
of penis. The lesion began as a papule about 3 weeks earlier and slowly progressed to form the
ulcer. It was painless, and the patient noticed no pus or discharge from the ulcer. On asking
further he mentions that he is sexually hyperactive with multiple unknown new sexual
partners, and he does not like to use any condoms during sexual intercourse.
He is a chronic alcoholic and smoker, living single and has lost his family in an accident. He
spends his weekend time with his friends. Before this the patient had consulted a Genito-
urinary disease specialist for a sexually transmitted disease (he had suffered from multiple
ulcers on shaft of penis which were fluid filled vesicles before proceeding to painful ulcers
which subsided naturally and not followed up after that. t. He is also suspected of trading
drugs for sex based on his criminal records.

Clinical examination showed the patient’s temperature was 37°C, pulse 80/min, respiratory
rate- 16/min, and blood pressure of 110/80 mm Hg. There was circular ulcer on shaft of penis
measuring 1 x2 cm (about 0.79 in). The ulcer had a clean base and raised borders with
moderate induration. There was little pain on palpation. Left inguinal lymph nodes were
palpable. All other systems (CVS, GIT, Respiratory system, Renal system) appear to be
normal.

Anatomy:
Local examination:
• The patient was circumcised. The glans penis was normal, and the urethral meatus was
at the tip of penis.
• On the left side of dorsal surface of shaft of the penis, there was a 1 cm ulcer. The ulcer
had a clean base and raised borders with moderate induration.
• The ventral surface of the penis was absolutely normal.

Q1. In this case which group of lymph nodes will be affected?

Superficial inguinal nodes.

Q2. Describe the lymphatic drainage of the penis:

1. Lymphatic from the glans penis drains into deep inguinal LN. and external iliac LN.
2. Lymphatic from superficial tissues of the of the penis drain into superficial inguinal
nodes.

Q3. The pain sensation from the ulcer area is transmitted through which nerve?
Dorsal nerve of penis branch of Pudendal nerve

Physiology: NA

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Biochemistry: NA

Pharmacology

Q4. What is the drug of choice for the eradication of uncomplicated gonorrhea?
Single dose of injection ceftriaxone 500 mg IM.
If chlamydia has not been excluded, treatment with doxycycline 100 mg twice a day for 7 days
is added.

Q5. How will you treat a case of complicated gonorrhea?

Inj. ceftriaxone 1 g IM or IV every 24 hours for at least 7 days, in addition to a single oral
azithromycin dose of 1 g.

Q6. What instructions should be given to the patient during the treatment?
The patient should avoid sexual activity for 7 days
All the sexual partners should be treated simultaneously even if they are asymptomatic

Microbiology:
Q7. What are the Risk factors for STDs?
• 4 STIs are incurable viral infections: HIV, HBV, HSV, HPV
• Age <25 years (young age)
• Multiple sexual partners
• Failure to use barrier contraception
• Unnatural sexual practices (oral, anal, MSM, WSW)
• Lower socioeconomic status (prostitution)
• Illiteracy, ignorance, illicit drug use (alcohol, heroin. etc. )
• Peer influence or environment
• Other associated STDs

Q8. Name the possible organisms that can cause Genital ulcer.
Herpes simplex 1,2 , Syphilis, C. trachomatis L1,2,3 [LGV], H. ducreyi, K. granulomatis

Q9. Name the various viruses that can cause STD.

HIV, HBV, HPV, HSV

Q10. Name the different bacteria that can cause STDs.

Treponema pallidum, Gonococci, C. trachomatis L1,2,3 [LGV], H. ducreyi, K.
granulomatis

Q11. What is the causative agent of chlamydia, gonorrhea, syphilis, soft chancre and
Donovanosis?
H. ducreyi

Q12. What are Primary signs & symptoms of STDs?

• Asymptomatic especially in women
• Genital or Vulval irritation/pain or itching

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 • Ano-Genital ulcers or blisters- painless or painful
• Dysuria - more commonly in men
• Discharge - Abnormal vaginal, urethral, cervical
• Dyspareunia - genital pain during or after sex
• Warty lesions or growths on genital or perineum
• Genital itching
• Others (no genital lesions, lymphadenopathy)

Q13. What are the STDs caused by HPV, high risk types and what are complications of
HPV infection?
• Warts on the penis are usually multiple, and on the shaft are often flat and keratinized.
• Warts in the perianal area often extend into the anal canal.
• Warts in the vulvoperineal area can enlarge dramatically and extend into the vagina.
• Cervical dysplasia caused by papillomavirus
• 14 high-risk HPV types 16, 18, 31, 33, 35, 39, 45, 51, 52, 56, 58, 59, 66, and 68
• Cervical cancer, vaginal, Anal, penile, vulval cancer - HPV 16 &18 found in 64-79%

Medical Parasitology:

Q14. What are sexually transmitted parasites?

sexually transmitted parasites are: (1) Trichomonas vaginalis (2) Phthirus pubis (3) Sarcoptes
scabiei

Q15. Mention the infective stages, diagnostic stage and lab diagnosis of each one of them?

Infective stage Diagnostivae stage Lab diagnosis

Trichomonas Trophozoites Microscopy: Detect motile
vaginalis trophozoites (darting movement) in
wet film - culture
-Immunoassay: detect antigen (RDT)
-NAAT: detect DNA (PCR)
Phthirus Adult lice Adult lice Demonestrate Adult lice or Nits (lice
pubis Lice egg (nit) eggs) in pubic hair by magnifying
lense, microscope
Sarcoptes Adult Sarcoptes Adult Sarcoptes Detect parasite [mite or mite products
scabiei scabiei mite scabiei mite or mite (eggs, faeces)] in:
products (eggs, (1) opened tunnel (by needle) using
faeces) magnified lens,
(2) skin scrap using microscope or
(3) Dermo-scopy

25
Q16. Can sexually transmitted parasites cause infertility? Explain?

Yes, only Tichomonas vaginalis by producing pelvic and tubual inflammation → tubal
obliteration → 2ry tubal infertility.

Clinical Skills:
Complaining from lower abdominal pain, severe burning sensation during urination for
many days. Additionally, he was suffering from penile cloudy discharge and testicular
tenderness.

Q17. Which of the following methods of the contraception provides the highest level of
protection aganist sexually transmitted infection (STI)?
1. Barrier methods (Answer)
2. Hormonal methods
3. Intrautrine devices
4. Fertility awareness based methods

Q18. What are the investigation required for diagnosis of sexually transmitted infection
(STI) in males?

First pass urine PCR and urethral swab

Reading Material Case IV: Sexually Transmitted Diseases (STD)

Anatomy:
• Gray’s Anatomy for students
• Clinical Anatomy for medical students (Richard Snell)

Pharmacology:

• Basic & Clinical Pharmacology by BG Katzung 15e Ch 43/44

• Goodman & Gillman’s pharmacological basis of therapeutics 14e Ch 57/59
• [Link]

Microbiology:
• Students're requested to refer slides and referral material

Clinical Skills:
• Talley, NJ & O'Connor, S 2006 Clinical Examination: A systematic guide to physical
diagnosis 5th ed MacLennan & Petty Sydney Ch 1 pg 10-11 (systems review), Ch 4 & 6
• Epstein, O, Perkin, GD, de Bono, DP & Cookson, J 2008 Clinical Examination 4th ed
Mosby, Edinburgh Ch 7, 8 & 9

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 Case V: Erectile dysfunction (ED)
Learning Objectives: Student will be able to

Anatomy:
• Understand the anatomy of the penis.
• Blood supply and lymphatic drainage of penis.
• Nerve supply of penis.

Physiology:
• Understand the components of the male sex act.
• Understand the erection reflex.

Biochemistry: NA

Pharmacology:
• Discuss the actions, uses, ADRs, contraindications, precautions, and interactions
of drugs used to treat erectile dysfunction.

Microbiology: NA

Clinical Skills: NA

Case Scenario+ questions: Erectile dysfunction (ED)

Mr. Hamed, a 62-years old, Saudi government employee, heavy smoker and live a sedentary life
with apparent obesity joins the clinic of his primary care physician Dr Salih as he complains of
erectile dysfunction disease. After history taking and examination the doctor inquiries about
other aspects of his health. Mr. Hamed mentioned that it has become increasingly difficult for
him to achieve a firm erection for enough time to complete the sexual intercourse. Dr Salih
referred him to the urologist consultant Dr Yasser to find out the cause and the proper treatment
procedures for him. After history taking and full examination of penis, prostate, scrotum and
testis, Dr Yasser ordered following investigations for Mr. Hamed:

1- Hormonal assays including the following hormones:

a. Total and free testosterone found slightly decreased than normal but expected in this age.

b. Full thyroid gland functions: Found normal

c. FSH and LH; found normal.

d. Prolactin found normal.

27
2. Full blood picture: found normal.

3. Full serum lipogram: showed an increased level of total cholesterol, LDL-cholesterol

And triglycerides.

4. Fasting and PP blood glucose levels found normal.

5. CT scan for the lumbar and sacral vertebrae: showed slight degenerative changes.

[Link] Doppler Sonography PDS: Showed Decreased blood flow in the cavernous

Arteries by 25%.

The final etiology was found to be a vascular atherosclerotic change in the penile arteries

So, Dr Yasser gave him the treatment of atherosclerosis including hypolipidemic drug e.g
Lipostat. With the traditional drugs in this case: selective inhibitors of PDE5 (Sildanfil). He also
advised him to perform regular exercise and to reduce his body weight.

Anatomy:
Erectile dysfunction possibly generates from any process that impairs either the neural or the
vascular pathways that contribute to erection. Neurogenic erectile dysfunction is caused by a
deficit in nerve signaling to the corpora cavernosa.

Q1. [Link] was found to have atherosclerotic changes in the arteries. Name the
arteries suppling the penis.
1. Dorsal artery
2. Deep artery of penis
3. Artery of bulb of penis

Q2. Name the branch of the artery which pours blood into the cavernous spaces.
Helicine artery.

Q3. In case of neurogenic erectile dysfunction which nerve would be affected?

Parasympathetic nerve (nervi erigentis, S2-S4)

Q4. Which specific structures in the penis are involved in achieving and maintaining an
erection?
The corpora cavernosa are two chambers inside the penis that fill with blood and become
engorged during an erection.

Q5. Can abnormalities or conditions affecting the nerves or blood vessels in the pelvic
region contribute to erectile dysfunction?

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YES, Conditions such as diabetes, high blood pressure, cardiovascular disease, and neurological
disorders can all impact the blood flow and nerve function required for an erection.

Q6. Mention anatomical factors that can increase the risk of developing erectile
dysfunction:
Structural abnormalities or damage to the blood vessels, nerves, or tissues involved in the
erectile process. Examples include Peyronie’s disease, which causes abnormal curvature of the
penis, and surgical procedures that may damage the nerves or blood vessels in the pelvic region.

Physiology:

Q7. The components of the male sex act include:

Erection, Ejaculation (Emission phase, Expulsion phase)

Q8. Which components of the male sex act are a spinal reflex?
Erection and ejaculation

Q9. How is the mechanism of the two phases of ejaculation differ?

Emission: Sympathetically induced contraction of the smooth muscle in the walls of the ducts
and accessory sex glands.

Expulsion: Motor-neuron-induced contraction of the skeletal muscles at the base of the penis

Q10. By which mechanism the parasympathetic stimulation cause relaxation of penile

arteriolar smooth muscle?
By nitric oxide, which causes arteriolar vasodilation in response to local tissue changes
elsewhere in the body.

Q11. Can a paralyzed man due to a higher spinal cord injury complete the erection reflex?
Why?

Yes he can complete the erection reflex as long as the spinal reflex arc remains intact
(Erection generating center lies in the lower spinal cord).

Q12. Complete the missing steps in the erection reflex:

29
 Parasympathetic supply to Parasympathetic
Sympathetic supply
bulbourethral and urethral supply to penile
to penile arterioles
glands arterioles

Penile arterioles dilate

Lubrication

Compresses veins

Biochemistry: NA

Pharmacology:
The patient was advised to quit smoking and to reduce the body weight. He was prescribed
rosuvastatin and sildenafil citrate with a follow-up appointment.

Q13. What is the first line for erectile dysfunction?

Phosphodiesterase-5 inhibitors

Q14. Write the mechanism of actions of the above-mentioned drugs?

30
Inhibition of PDE-5 → ↑↑cGMP

➢ Protein kinase-G activation that leads to vasodilation

➢ Accumulation of blood in the corpus cavernosum resulting in penile erection
➢ Enhances the normal erectile response to sexual stimuli.

Q15. List other uses of PDE-5 inhibitors?

Pulmonary arterial hypertension (improve arterial oxygenation)

Q16. List contraindications to the use of PDE-5 inhibitors?

Recent cardiovascular events, on organic nitrates, Peronei's disease, cavernosal fibrosis, liver &
kidney diseases

Q17. Give reasons why PDE-5 inhibitors should not co-administered with drugs like
organic nitrates and alpha-1 adrenergic blockers?

Severe hypotension & MI can occur

Microbiology: NA
Clinical Skills: NA

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Reading Material Case V: Erectile dysfunction (ED)

Anatomy:
• Gray’s Anatomy for students
• Clinical Anatomy for medical students (Richard Snell)

Physiology:

• Sherwood, Human Physiology from cell to system, (9th edition, Ch. 20, page 732-734)

Pharmacology:
• Rang & Dale's Pharmacology, 10th Edition Ch 36
• Goodman & Gillman’s pharmacological basis of therapeutics 14e Ch 45
• [Link]

32