GASTROENTEROLOGY

Dysphagia:★★
Dysphagia is defined as difficulty in swallowing.

Causes:
A) Oropharyngeal causes:
Oropharyngeal disorders result from neuromuscular dysfunction affecting the initiation of
swallowing by the pharynx and upper oesophageal sphincter e.g.
1. Bulbar palsy
2. Pseudobulbar palsy
3. Myasthenia gravis
B) Oesophageal causes:
Stricture:
1) Benign:
● Peptic
● Fibrous rings.
2) Malignant:
● Carcinoma of the oesophagus.
● Carcinoma of the stomach.
● Extrinsic compression.
Oesophagitis:
1) Peptic
2) Candidiasis
3) Eosinophilic
Dysmotility:
1) Achalasia
2) Nonspecific motility disorder

Dyspepsia:★★
Dyspepsia (indigestion) is a collective term for any symptoms thought to originate from the
upper gastrointestinal tract.

Alarming features of dyspepsia:★★

1) Weight loss.
2)Anaemia.
3) Vomiting.
4) Haematemesis and/or melaena.
5) Dysphagia.
6)Palpable abdominal mass.

Causes of upper GIT bleeding:★★★

1) Peptic ulcer (Gastric ulcer & duodenal)
2) Gastric erosions
3)Oesophagitis.
4)Rupture of oesophageal or gastric varices
5) Mallory-Weiss tear
6) Vascular malformation
7) Cancer of stomach or oesophagus
8) Aorto-duodenal fistula

Diarrhoea:★
Passage of loose stool(more than three times a day is called diarrhoea.

Types of diarrhoea:
According to duration:★★
1) Acute diarrhoea: Diarrhoea persisting less than 14 days.
2)Chronic diarrhoea: Diarrhoea persisting more than 14 days.
According to nature:
A) High volume diarrhoea: (> 200 gm stool/day or > IL per day)
B) Low volume diarrhoea: (< 200 gm stool/day).

Causes of acute watery diarrhoea:★★

Infectious causes:
1) Bacterial toxin : Toxin of Staphylococcus aureus, Clostridium botulinum, Bacillus cereus
2) Bacteria : Vibrio cholerae, E. coli, Shigella, Campylobacter jejunii, Salmonella speci.
Clostridium perfringens, Clostridium difficile, Yersinia.
3)Virus :Rota virus (most common), Astro virus, Calci Virus, Adeno virus, Corona virus,
Norwalk virus. (Remember: RACNA)
4) Parasites : Entamoeba histolytica, Giardia lamblia,

Aphthous ulcer:★
Aphthous ulcers are superficial and painful; they occur in any part of the mouth.
Occurrence:
Recurrent ulcers afflict up to 30% of the population and are particularly common in women prior
to menstruation.
Cause:
Usually unknown
Premenstrual
Diagnosis:
Clinical.
Occasionally biopsy is necessary for diagnosis.
Treatment:
Topical corticosteroids (such as 0.1% triamcinolone in Orabase) or choline salicylate (8.7%)
gel.
Symptomatic relief is achieved using local anaesthetic mouthwashes.
Gastro-oesophageal reflux disease:★★★
Gastro-oesophageal reflux disease develops when the oesophageal mucosa is exposed to
gastro-duodenal contents for prolonged periods of time, resulting in symptoms and, in a
proportion of cases,oesophagitis.

Factors responsible for GERD★★

● Obesity
● Diet: Dietary fat, chocolate, alcohol
● Defective oesophageal clearance.
● Abnormal lower oesophageal sphincter (reduced tone, inappropriate relaxation).
● Delayed gastric emptying.
● Increased intra-abdominal pressure.
● Hiatus hernia.
(Remember : Obese HADDDI)

Clinical features:
1) Heartburn and regurgitation provoked by bending, straining or lying down.
2) Waterbrash.
3) The patient is often overweight.
4) Woken at night by choking as refluxed fluid irritates the larynx.
5) Odynophagia or dysphagia.
6)Atypical chest pain, which may be severe, can mimic angina and is probably due to reflux-
induced oesophageal spasm.

Peptic ulcer disease / PUD:★★★

Peptic ulcers are acute or chronic, most often solitary lesion that occur in any portion of the
gastrointestinal tract exposed to aggressive action of acid peptic juices.

Common sites of peptic ulcer★★★

(খুবই গুরুত্বপূর্ণ)
1) First part of duodenum.
2) Stomach (Usually antrum).
3) Lower oesophagus.
4) Within the margins of a gastro-jejunostomy.
5) Throughout GIT in Zollinger-Ellison syndrome.
6)Within or adjacent to an ileal Meckel's diverticulum that contains ectopic gastric
mucosa.

Causes of peptic ulcer disease ★★

1) H. pylori.
2) Drugs:NSAIDs, steroids.
3) Smoking.
4) Alcohol.
5) Stress: Psychological, burn,CVD.
6) Reduced mucosal blood flow: Ischaemia, shock.
7) Over-production of gastric HCI: Gastrin producing tumours as in Zollinger Ellison syndrome.

Complications of peptic ulcer disease:★★★

1) Perforation: Occurs in about 5% of patients, accounts for two thirds of ulcer deaths
2) Gastric outlet obstruction: Occurs in about 2% of patients.
3) Bleeding:Occurs in 15 - 20% patients, may be life-threatening

Investigations of peptic ulcer disease:★★

1) Upper GI endoscopy. A biopsy should be taken to exclude malignancy.

2) Test for H Pylori:
Non invasive:
Serology
Urea breath tests
Faecal antigen test
Invasive (antral biopsy):
Histology
Rapid urease tests, e.g. CLO, Pyloritek
Microbiological culture

Helicobacter pylori / H. pylori:★★

H. pylori is Gram-negative spiral bacillus and has multiple flagella at one end which make
it motile,allowing it to burrow and live deep beneath the mucus layer closely adherent to the
epithelial surface.

Mode of transmission:
The bacteria spread by person-to-person contact via gastric refluxate or vomit.

Habitats:
Exclusively gastric-type epithelium.
Duodenum.
Patches of gastric metaplasia.

Diseases caused by H. pylori:★★

1) Gastritis.
2) Duodenal ulcer.
3) Gastric ulcer.
4) Gastric cancer.

Mechanism of disease process:

Secretes urease enzyme which breaks down urea and form toxin compound ammonium
chloride and monochloramine.

Malabsorption syndrome:★★
Malabsorption syndrome is characterized by diarrhoea and weight loss in a patient with normal
diet,and results from impaired absorption of nutrients from the small intestine.

Causes of malabsorption:★★
1) Deficiency of bile or pancreatic enzymes,Fat and protein malabsorption results.
2) Bacterial overgrowth.
3)Small bowel resection.
4) Conditions damaging the small intestinal epithelium, such as:
● Coeliac disease.
● Tropical sprue.
● Dermatitis herpetiformis.
● Whipple's disease
● Radiation enteritis.
● Parasitic infestation (e.g. Giardia intestinalis)

Intestinal TB:
Organism responsible for abdominal tuberculosis / intestinal TB
Mycobacterium tuberculosis★★★

Sites:
● The area most commonly affected is the ileocaecal region.
● TB can affect any part of the gastrointestinal tract.
● Peritoneal TB may result in peritonitis and exudative ascites.
● Liver - Grannulomatous hepatitis.

Management of intestinal tuberculosis:★

Clinical features:
● Abdominal pain
● Low-grade fever.
● Night sweats.
● weight loss
● Features of anaemia (tiredness, palpitation)
● Alteration of bowel habit.
● Features of intestinal obstruction - Constipation vomiting.
● Abdominat swelling - If ascites due to peritoneal involvement
● Palpable abdominal mass, specially in right iliac fossa.
Investigations:
1) ESR - Raised.
2) Barium follow through
3) USG and CT shows mesenteric thickening and lymph node enlargement
4) Serum alkaline phosphatase - Increased suggests hepatic involvement
5) Confirmation is sought by endoscopy, laparoscopy or liver biopsy

Treatment:
1)Chemotherapy with four drugs: Isoniazid, rifampicin, pyrazinamide & ethambutol.
2) Treatment should last 1 year.

IBD
Factors associated with inflammatory bowel disease:★★
Environmental:
1) UC is more common in non-smokers and ex-smokers.
2) CD more common in smokers
3) CD associated with low-residue, high refined sugar diet.
4)Commensal gut microbiota altered (dysbiosis) in CD & UC.
5)Appendicectomy protects against UC.

Comparison between ulcerative colitis and Crohn’s disease ★★

1) Age group: Any age group both for UC & Chrons disease.
2)Gender: in UC, M = F but in CD Slight female preponderance
3)Incidence:In UC Stable but in CD is Increasing
4) Ethnic group: In UC Any & in CD Any; more common in Ashkenazi Jews
5)Genetic factors: in UC HLA-DR*103; colonic epithelial barrier function (HNF4α, LAMB1,
CDH1)& in CD,Defective innate immunity and autophagy (NOD2, ATG16L1, IRGM)
6)Risk factors: UC More common in non-/ex-smokers Appendicectomy protects but CD More
common in smokers
7)Anatomical distribution: UC in Colon only; begins at anorectal margin with variable
proximal extension but CD occurs in Any part of gastrointestinal tract; perianal disease
common; patchy distribution, skip lesions
8)Extra-intestinal manifestations: Common for both UC & CD
9)Presentation:in UC Bloody diarrhoea but in CD Variable; pain, diarrhoea, weight loss all
common
10)Histology: In UC Inflammation limited to mucosa; crypt distortion, cryptitis, crypt abscesses,
loss of goblet cells but in CD Submucosal or transmural inflammation common; deep fissuring
ulcers, fistulae; patchy changes; granulomas.
11) Management: For UC 5-ASA; glucocorticoids; azathioprine; biological therapy (anti-TNF,
anti-α4β7 integrin); colectomy is curative Glucocorticoids but for CD azathioprine;
methotrexate; biological therapy (anti-TNF, anti-α4β7 integrin); nutritional therapy; smoking
cessation; surgery for complications is not curative; 5-ASA is not effective
IBS
Features supporting a diagnosis of IBS:★★
● Symptoms > 6 months.
● Frequent consultations for non-GI problems.
● Previous medically unexplained
symptoms.
● Stress worsens symptoms.

Alarming features of IBS:★★★

● Age > 50 years: male gender.
● Weight loss.
● Nocturnal symptoms.
● Family history of colon cancer.
● Anaemia
● Rectal bleeding.

Management of irritable bowel syndrome:★★

Clinical features:
Gastrointestinal features:★★
1) Recurrent colicky abdominal pain.
2) Altered bowel habit.
3) Abdominal distension,
4) Rectal mucus.
5) Feeling of incomplete defecation

Non-gastrointestinal features:
A) Gynaecological:
● Painful periods (dysmenorrhoea).
● Pain following sexual intercourse (dyspareunia)
● Premenstrual tension
B) Urinary:
● Frequency
● Urgency
● Nocturia
● Incomplete emptying of bladder.
C) Others:
● Back pain.
● Headaches.
● Bad breath, unpleasant taste in the mouth
 ● Poor sleeping.

Investigations:
To exclude other diseases.
1) Full blood count
2) Sigmoidoscopy
3) Colonoscopy in older patients or all patients having a rectal bleeding to exclude colorectal
cancer
4) In diarrhoea predominant patients, investigations to exclude
a. Microscopic colitis
b. Lactose intolerance

Treatment of IBS: ★
A) Reassurance.
B)Diarrhoea predominant:
● Avoid legumes and excessive dietary fibre.
● Consider trials of low FODMAP or gluten free diet.
● Anti-diarrhoeal drugs: Loperamide 2-8 mg daily
● Amitryptyline / Imipramine 10 - 25 mg daily at night.
● Rifaximin 600mg daily for 2 weeks.
C) Constipation predominant:
● High-roughage diet.
● Ispaghula or psyllium.
● Lactulose and macrogol.
● lubiprostone can be effective.
D) If still symptoms persist -
● Duloxetine 30 - 60 mg at night.
● Relaxation therapy.
● Biofeedback.

Functional dyspepsia / non-ulcer dyspepsia:★★

This is defined as chronic dyspepsia (pain or upper abdominal discomfort) in the absence of
organic disease.
Subgroup:
Ulcer-like
Dysmotility-type
Aetiology:
Mucosal disorder
Motility disorder
Psychiatric disorders
Clinical features:
>Patients are usually young (<40 years).
>Women are affected twice as commonly as men.
>Nausea
> Early satiety.
>Fullness.
>Bloating after meals.
> Morning symptoms are characteristic & pain or nausea may occur on walking.
Investigations:
1) All patients should be checked for H. pylori infection.
2) Patients over 55 years should undergo endoscopy to exclude mucosal disease.
3)ultrasound scan to detect gallstones
Treatment:
1)The most important elements are explanation and reassurance.
2) Up to 10% of patients benefit from H. pylori eradication therapy & this should be offered to
infected patients.
3) Fat restriction may help.
4) Antacids (sometimes helpful).
5) Prokinetic drugs: Metoclopramide (10 mg 8-hourly) or Domperidone (10-20 mg 8-hourly)

Causes of acute pancreatitis:★★

A) Common★★★ (90% of cases):
1) Gallstones.
2) Alcohol.
3) Idiopathic
4) Post-ERCP
(Remember : GAPI)
B) Rare:
1) Post-surgical: Abdominal, cardiopulmonary bypass.
2)Trauma.
3) Drugs: Azathioprine / Mercaptopurine thiazide diuretics.
4) Metabolic: Hypercalcaemia, hypertriglyceridaemia.
5) Pancreas divisum.
6) Sphincter of Oddi dysfunction
7)Infection (mumps, Coxsackie virus),
8) Hereditary

Management of acute pancreatitis:★★

History of following:
Alcohol intake
Gallstone disease
ERCP
Drugs: Thiazide diuretics, sodium valproate.
Abdominal surgery.
Trauma to the abdomen.
Clinical features:
1) Upper abdominal pain:characteristics
-Şevere Constant &Radiates to the back in 65% cases
-Persists for hours or even days.
-Agonizing.
-Refractory to usual analgesics.
-Is relieved by knee-elbow position.
- Discoloration of the flanks (Grey Turner's sign) or the peri-umbilical region (Cullen's sign).
Investigations:
1) Elevation of serum amylase or lipase concentrations.
2) Ultrasound or CT: Evidence of pancreatic swelling.
3) Elevated urinary amylase: creatinine ratio.
4)Persistently elevated serum amylase concentration suggests pseudocyst formation
5) Blood urea and serum electrolytes.
6) Blood glucose level - May be elevated. Treatment:
1)Analgesics: Opiate analgesic Pethidine should be given.
2)Hypovolaemia: Correction of hypovolaemia using normal saline &/or colloids.
3) Oxygen should be given in hypoxic patients.
4) Nasogastric aspiration if paralytic ileus is present.
5) Hyperglycaemia: Corrected by using insulin.
7) Correction of hypocalcaemia by intravenous calcium injection if tetany occurs.

Complications of acute pancreatitis:★★

Systemic:
1) Systemic inflammatory response syndrome (SIRS).
2) Hypoxia.
3) Hyperglycaemia.
4) Hypocalcaemia.
5) Reduced serum albumin concentration.
Pancreatic:
1) Necrosis.
2) Abscess.
3) Pseudocyst.
4) Pancreatic ascites or pleural effusion.
GIT:
1) Upper gastrointestinal bleeding.
2 Variceal haemorrhage.
3) Erosion into colon.
4) Duodenal obstruction
5) Obstructive jaundice.

NEPHROLOGY

Polyuria:★★
Polyuria means an inappropriately high urine volume > 3 litres/day.
Cause of Polyuria:
1) Excess fluid intake.
2) Hyperglycaemia
3) Cranial Diabetes insipidus (reduced ADH secretion).
4) Nephrogenic diabetes insipidus (tubular dysfunction):
Lithium or diuretics.
Interstitial nephritis.
Hypokalaemia.
Hypercalcaemia.

Haematuria:★★
Haematuria is the presence of red blood cells in the urine due to bleeding from the kidney or
urinary tract.
Causes of haematuria:
According to site of involvement of pathology:
A) Systemic / pre-renal:
1)Purpura
2) Sickle cell trait
3) Bleeding disorders, including anti-coagulant drugs
B) Renal:
1) Infarct / papillary necrosis
2) Trauma
3) Tuberculosis
4) Stones
5) Renal pelvis transitional cell carcinoma,
C) Post-renal:
1)Ureteric stones
2) Ureteric neoplasms
3) Bladder tumours (transitional cell carcinoma)
4) Bladder tuberculosis and bilharziasis
5) Radiation cystitis
6) Drug-induced cystitis, e ciclophosphamide
7) Prostatic enlargement
8) Urethral neoplasms

Massive proteinuria:★★★
When more than 3.5 gm albumin passes through urine in 24 hours, it is called massive
proteinuria.
Causes of massive proteinuria
1) Nephrotic syndrome
2) Amyloidosis
3) Multiple myeloma
4) Toxaemia of pregnancy
Urinary tract infection / UTI:★★★
UTI is defined as multiplication of organisms in the urinary tract. It is usually associated with the
presence of neutrophils and > 10^5 organisms/ml in a midstream sample of urine (MSU).
Etiology:
Organisms causing UTI in the community include:
>Escherichia coli derived from the gastrointestinal tract (about 75% of infections).
>Proteus.
>Staphylococcus saprophyticus or Staph. epidermidis
>Klebsiella,
>Pseudomonas species.
Risk factor for urinary tract infection:
A)Incomplete bladder emptying:
- Bladder outflow obstruction.
- Neurological problems (eg, multiple sclerosis, diabetic neuropathy), Spina bifida
- Gynaecological abnormalities (e.g. uterine prolapse).
- Vesico-ureteric reflux.
B)Foreign bodies:
Urethral catheter or ureteric stent.
C) Loss of host defenses:
-Atrophic urethritis and vaginitis in post-menopausal women
-Diabetes mellitus

Management of urinary tract infection:★★

Clinical features
1) Abrupt onset of frequency of micturition.
2) Scalding pain in the urethra during micturition (dysuria).
3) Supra-pubic pain during and after voiding.
4) Intense desire to pass more urine after micturition, due to spasm of the inflamed bladder wall.
Urine may appear cloudy and have unpleasant odour.
6) Microscopic or visible haematuria.
7) Systemic symptoms: Fever with chill & rigor.
Investigations of UTI:
1) Culture of MSU, or urine obtained by supra-pubic aspiration
2) Microscopic examination
3) Dipstick examination of urine for blood, protein and glucose.
4) Full blood count.
5) Plasma urea, electrolytes, creatinine.
6) Blood culture.
Treatment
Cystitis and uncomplicated UTI
Trimethoprim (1st choice)
Amoxicillin
Nitrofurantoin
Pyelonephritis and complicated UTI
Co-amoxiclav
Ciprofloxacin (1st choice)
Cefuroxime
Gentamicin
Recurrent urinary tract infection (recurrent UTI):★★
>If the causative organism persists on repeat culture despite treatment, or if there is reinfection
with any organism after an interval, then an underlying cause is more likely to be present and
more detailed investigation
is justified.
>In womens recurrent infections are common Prophylactic therapy:
Trimethoprim
Nitrofurantoin
Co-amoxiclav
Advice:
1) Fluid intake at least 2 L/day.
2) Regular complete emptying of bladder.
3) Good personal hygiene.
4) Emptying of bladder before and after sexual intercourse.
6) Cranberry juice may be effective.

Acute pyelonephritis:★★
Acute inflammation of the kidney and renal pelvis is known as acute pyelonephritis.
Clinical features:
Classical triad:★★★
Loin pain (radiate to the iliac fossa and suprapubic region)
Fever (with rigor).
T'enderness over the kidneys.

Others:
Dysuria due to associated cystitis.
Vomiting.

Investigation:
1) Culture of MSU, or urine obtained by Suprapubic aspiration.
2) Microscopic examination or cytometry of urine for white and red cells.
3) Dipstick examination of urine for blood, protein and glucose.
4) Full blood count.
5) Plasma urea, electrolytes, creatinine.
6) Blood culture.

Treatment:
Adequate fluid intake.
Antibioties:
Co-amoxiclav (1st choice)
Ciprofloxacin (1st choice)
Cefuroxime
Gentamicin
For 10 to 14 days duration

AGN/ Nephritic syndrome:★★★

Acute nephritic syndrome is characterized by inflammation in the glomeruli which is manifested
as haematuria, red cell casts in the urine, azotemia, oliguria and mild to moderate hypertension.

Cardinal presentation of AGN:★★★

● Haematuria (red or brown urine).
● Oedema and generalized fluid retention.
● Hypertension
● Oliguria
● Proteinuria.

Clinical features of AGN:

Symptoms:
Fever (Low-grade).
Lethargy.
Anorexia, nausea, vomiting,
Generalized body swelling.
Abdominal pain.
Scanty micturition
High colored urine.
Signs:
Oedema.
Scratch mark may be present in skin.
BP: Increased.
Ascites.

Investigations:
● Urine analysis (RBC, RBC cast, mild proteinuria).
● Complete blood count (polymorphonuclear leukocytosis, normocytic normochromic
anaemia).
● Serum C3 level (reduced).
● Evidence of streptococcal infection
● Serum creatinine (may be raised).
● Blood urea (may be raised).

Treatment:
No specific treatment, mainly supportive & symptomatic.
1. In mild case:
Bed rest and careful monitoring of blood pressure.
K+ containing fruit restriction.
Fluid and salt restriction.
Diuretics if edema is massive.
2.In severe case:
Fluid restriction for ARF
Correct electrolyte and acid base balance
Treat hypertension with nipedipine or labetalol
Antiobiotics eg. Penicillin

Causes of generalized oedema:★★★

(VERY IMPORTANT)
1) Nephrotic syndrome.
2) Congestive cardiac failure (CCF).
3) Cirrhosis of liver,
4) Protein-energy malnutrition.

Nephrotic syndrome:★★
It is a glomerular syndrome characterized by -(Commom features★★★)
1)Overt proteinuria: > 3.5 gm /24 hours (urine may be frothy).
2)Hypoalbuminaemia (<30 gm/L).
3) Oedema and generalized fluid retention.
4) Intravascular volume depletion with hypotension, or intravascular expansion with
hypertension may occur.

Causes of nephrotic syndrome:★

A) Primary glomerular causes:
● Membranous glomerulopathy.
● Minimal change disease.
● Focal segmentat glomerulosclerosis.
● Membrano proliferative glomerulonephritis.
B) Secondary /systemic cases:
● Systemic diseases: Diabetes mellitus, amyloidosis, SLE.
● Drugs NSAID penicillamine,street heroin
● Infections. Malaria, syphilis, hepatitis B&C, AIDS
● Malignant disease: Carcinoma, lymphoma
● Miscellaneous Allergy, hereditary nephritis

Clinical features of nephrotic syndrome:

Symptoms:
Generalised swelling of the body
Anorexia
Weakness
Abdominal pain
Diarrhoea
Burning sensation during micturition
Signs:
Pitting oedema (First periorbital) then generalized)
Blood pressure: Normal.
Anaemia (May be present)
Leuconychia (may be present)
Alimentary: Feature of ascites may be present.
Respiratory: Feature of bilateral pleural effusion.
Cardiovascular system: Feature of pericardial effusion.

Laboratory findings:
>Urinary findings:
Proteinuria: 3+/4+.
24 hr protein in urine: In children> Igm/M2/24hrs, in adult > 3.5gm/24hrs.
Hyaline cast
>In serum:
Serum cholesterol and triglyceride level >250 gm/dl.
Albumin <2. 5mg/dl.
Serum C3: normal.
>Renal biopsy in steroid-resistant cases
Treatment:
1. Supportive care:
Diet: Balanced diet adequate in protein and calorie
Fluid and salt are not restricted unless edema severe.
If edema is severe then diuretic is given.
Prophylactic daily oral penicillin against pneumococcal infection.
Treatment of complication
2. Specific
Initial attack Prednisolon 60mg/m2 body surface area daily (2-3 divided dose) for 6 weeks
Then, 40 mg/m2 body surface area single morning dose in alternate days for the next 6 weeks.

Complications of nephrotic syndrome:★★★

1)Hypoalbuminaemia.
2) Avid sodium retention.
3) Hypercholesterolaemia.
4) Hypercoagulability: Increase tendency to develop arterial and venous thromboembolism.
5)infection: Spontaneous peritonitis, pneumococcal sepsis, cellulitis, pneumonia, UTI.

Acute renal failure /ARF:★★

It refers to sudden and usually reversible loss of renal function, which usually develops over
days or weeks and usually accompanied by a reduction in urine volume.
Causes ARF :
a) Pre-renal causes:
Impaired perfusion due to-
1)Cardiac failure.
2 Sepsis.
3)Blood loss.
4)Dehydration
b) Renal causes:
1) Glomerulonephritis.
2) Small vessel vasculitis.
3)Acute tubular necrosis:
Drugs.
Toxin.
Prolonged hypotension.
4) Interstitial nephritis
Drugs.
Toxin.
Inflammatory disease.
Infection.
C) Post-renal causes:
1) Urinary calculi.
2) Retro-peritoneal fibrosis.
3) Benign prostatic enlargement.
4) Prostatic cancer.
5) Cervical cancer.
6) Urethral stricture

Chronic renal failure:★★

It refers to irreversible deterioration in renal function which classically develops over a period of
years.
Causes of CRF/CKD:★★★(MUST)
1) Diabetes mellitus
2) Interstitial Diseases
3) Glomerular diseases e.g. IgA nephropathy is most common.
4) Hypertension
5) Systemic inflammatory diseases e.g. SLE, vasculitis.
6)Congenital and inherited e.g. polycystic kidney disease, Alport's syndrome.
7)Renal artery stenosis (5%)

Features of CKD/CRF:★★
● A-Anaemia,
● B-Bony change.
● C-(CVS) HTN, uraemic
pericarditis, pulmonary oedema.
● D-Dermopathy, pruritus.
 ● E-(Endocrine)
-Hyperparathyroidism,
-Hyperprolactinaemia.
● F-(Fluid overload) Oedema.
● G-(GIT) Anorexia, nausea,
vomiting, hiccup
● H-(Haematological) Bleeding
manifestation
● I-Infection
● K-(Kidney) Polyuria, nocturia.
● M-Myopathy
● N-(Neurological)
Sensory- polyneuropathy
Motor- foot drop.

Diet in CKD:★★
Moderate restriction of protein (60gm/day) and adequate intake of calories to prevent
malnutrition.
Control of blood pressure and proteinuria:★★★
>Target blood pressure 130/85 mmHg (CRF alone)
>if proteinuria >lgm/day then target BP is 125/75mmHg
> Drug of choice: ACE inhibitors.

Causes of anaemia in CRF:★★★

1)Relative deficiency of erythropoietin.
2) Diminished erythropoiesis due to toxic effects of uraemia on marrow precursor cells.
3) Reduced red cell survival.
4) Increased blood loss due to capillary fragility and poor platelate function.
5) Reduced dietary intake and absorption and utilization of iron.

Renal osteodystrophy:★★
It is a metabolic bone disease in CRF consists of :
-Osteomalacia
-Hyper parathyroid bone disease (osteitis fibrosa)
-Osteoporosis
-Osteosclerosis

STD

Sexually transmitted bacterial infections★★

● Syphilis
 ● Gonorrhoea
● Chlamydial infection
● Other sexually transmitted bacterial infections

Sexually transmitted viral infections★★★

● Genital herpes simplex
● Human papillomavirus and anogenital warts
● Molluscum contagiosum
● Viral hepatitis

NEISSERIA GONORRHOEA:★★
>Transmitted sexually
>Newborn can be infected during birth
>Cause diseases only in human
>Gonococci affects only columnar cell.

Habitat:
Man is the only host, strict parasite and found in the discharge of lesion
Toxins and enzymes:
No exotoxin
i. Endotoxin
ii. Catalase
iii. Oxidase.
Clinical features of Gonorrhea:★★
Gonorrhea is symptomatic in men, Women is asymptomatic (80% cases).
Urethritis
Dysuria
Female-cervicitis (endocervix)
Complications:★★
● Salphingitis
● PID
● Sterility
● Ectopic pregnancy
Newborn:
Septic arthritis
Purulent conjunctivitis
Lab Diagnosis:
Gram (-) ve diplococci within PMNs (gm stain)
Culture - Thayer martin media
Rx-
Ceftriaxone /Ciprofloxacin
Causes of Non-Gonococcal Urethritis:★★★
1) C. trachomatis (type D-K)
2) U. urealyticum
3) Mycoplasma
4) Gardnerella vaginalis
5) Acinetobacter
6) HSV-2
7) Trichomonas vaginalis
8) Candida albicans.

Causes of sterile Pyruia★★★

a) 5T (Tumor, Trauma, TB, Treatment with
antibiotic, stone)
b) Viral infection
c) Parasitic infection
d) Fungal infection
e) Infection with atypical organism
e.g: Mycoplasma, Chlamydia, Rickettsiae

Treponema pallidum:
Characteristics
1)Thin walled, flexible motile rods
2. Not grown in cell culture of artificial media.
3. Non-pathogenic treponema → Part of normal flora of human mucous membrane can be
cultured.
4. Grows very slowly, does not produce any toxin & enzyme
5. Human is only natural host
6. Can penetrate the intact mucosa

TRANSMISSION:★★
• Intimate contact with infected person
• Homosexual
• Vertical/Transplacental
• Rarely blood transfusion

DISEASES:
Syphilis may be endemic & venereal.
Primary syphilis
|
Bacteremia
|
2ndary syphilis★★
-1/3 cure without Rx
- 1/3 → Latent
- ⅓ tertiary
Latent Syphilis
• Early latent: infections to others. (1-2yrs)
• Late latent - Non-infections
Primary Syphilis & Differences between chancre & chancroid:★★★
>Chancre formation → Chancre is single, painless, indurated and don't bleed on touch.
>multiple lesions are seen rarely and anal chancres are often painful. It heals spontaneously.
(Chancroid, caused by Haemophilus ducrey, is single or multiple painful ulcers with ragged
undermined edges)
Secondary Syphilis:
1. Maculopapular rash on palm & sole
2. Moist papule-on skin & mucous membrane e.g. sore throat
3. Condylomata lata → moist lesions on genitalia, highly infectious
4. Patchy alopecia
5. Constitutional symptoms- fever, generalized lymphadenopathy (more than 50% cases)
6. Snail track ulcer
Tertiary Or Late Syphilis:
1. Gumma formation in bones & skin, may be single or multiple.
2. CNS-Tabes paresis
3. CVS -Aortitis, Aneurysm
4. Nasal septum destruction occurs
5. In lesions-Treponema are rarely seen

Laboratory Diagnosis:
(a) Microscopy → DFA, dark field, silver stain
(b) Non-Specific serological test
Non-Specific Tests
VDRL,RPR
Specific Tests
> Becomes positive within (2-3) wks of
infection, remains positive for lifelong. So,
>Treponemal Ag is used
> ТРНА
>MHA-TP.
> Expensive, difficult to perform.
> Can't say prognosis.
PREVENTION:
No vaccine
Rx:
Penicillin, A single inj. Benzathine Panicillin

CAUSES OF GENITAL ULCERS:★★

. T. pallidum
• H. ducreyi
• HSV type 1 & 2, primarily type 1
• Calymmatobacterium/Klebsiella granulomatis
• C. trachomatis

Causes of vaginal discharge :★★

1) Candidiasis
2) Trichomoniasis
3) Bacterial vaginosis 4)Streptococcal/staphylococcal

Causes of urethral discharge :★★★

1) most important causes of urethral discharge are - gonorrhoea and chlamydia.
2)non-specific urethritis (NSU).
Trichomonas vaginalis, herpes simplex virus (HSV), mycoplasmas, ureaplasmas or
adenoviruses.

D/D of genital itch:★★

1)Subclinical urethritis
2) Candidiasis
3) balanitis
4)Lichen planus
5) Lichen sclerosus
6)Dermatoses, e.g. eczema or psoriasis
7) Genital herpes
8) Circinate balanitis

INFECTIOUS DISEASES

Pulmonary tuberculosis:★★★
Organisms responsible for tuberculosis:
● Mycobacterium tuberculosis
● Mycobacterium bovis
● Mycobacterium africanum

Primary pulmonary TB:

Primary TB refers to the infection of a previously uninfected (tuberculin-negative) individual.

Miliary TB:
(Blood-borne dissemination gives rise to miliary TB which may present acutely but more
frequently is characterized by 2-3 weeks of fever, night sweats, anorexia, weight loss and a dry
cough.
The classical appearances on chest X-ray are those of fine 1-2 mm lesions ('millet seed")

Post-primary pulmonary TB:

This refers to the infection of a previously infected(tuberculin positive) individual.

Management of pulmonary tuberculosis:★★

Symptoms:
-Chronic cough, often with haemoptysis
-Chronic low grade fever
-Evening rise of temperature
-Night sweats
-Anorexia
-Weight loss
Signs:
-Raised temperature,
-Patient may be cachectic.
-Cervical and other lymphadenopathy - When disseminated.
-Auscultation of chest is frequently normal.
-Features of complications e. g. pleural effusion,
Investigations:
1) CBC, ESR & Hb%: High rise of ESR, lymphocytosis, anaemia.
2) Chest X-ray: Patchy opacity.
3) Sputum or bronchoalveolar lavage for AFB: May be found by Ziehl-Neelsen staining.
4) PCR: Nucleic acid amplification.
5) Culture: (usually not done)
Solid media (Lowenstein-jensen), liquid(BACTEC)
6) Tuberculin test
7) Pleural fluid study (if there is pleural effusion): Including adenosine deaminase (ADA).

Treatment of TB (According to WHO):

Category of tuberculosis
Category 1
>New cases of smear +ve pulmonary TB.
>Severe extra-pulmonary TB.
>Severe smear -ve pulmonary TB.
Category-2
>Previously treated smear +ve PTB.
>Relapse.
>Treatment failure.
>Treatment after default.

Initial phase & Continuation phase

2 months HRZE &
4 months HR
H-isoniazide,R-rifampicin,Z-pyrazinamide,E-ethambutol.

★★Tuberculosis can occur in any part of our body except cardiac muscle,skeletal
muscle and thyroid gland.

MDR TB:★★★
It means multi-drug resistant tuberculosis.
WHO definition: A multi-drug resistance (MDR) strain is one that is at least resistant to
Isoniazid & Rifampicin.

Investigations:
>Gene Xpert.
>Drug sensitivity test.
Treatment:
Treatment of MDR tuberculosis can take at least two years and the results are poor.

XDR TB:★★
Extended drug resistant TB means resistance to INH & Rifampicin, fluoroquinolone & at
least one injectable 2nd line drug.

Indications of steroid (glucocorticoid) along with anti-TB drugs:

1)Absolute indication: Bilateral adrenal tuberculosis (replacement therapy).
2) Tubercular pericardial effusion (to prevent adhesion).
3) Tubercular meningitis (to prevent adhesion).
4) Tubercular pleural effusion (to prevent adhesion).
5)Tubercular peritonitis

Tubercular drugs with their side effects:

★★★
Isoniazide: Peripheral neuropathy, hepatitis,rash
Rifampicin: Hepatitis,GITupset,febrile reactions
Pyrazinamide:Hepatitis,hyperuricaemia,GIT upset.
Ethambutol:Retrobulbar neuritis
Streptomycin:8th nerve damage.

Leprosy:★★
Leprosy is caused by Mycobacterium leprae.characteristics of this organism is-
1.Also called HANSEN'S BACILLI
2. Has not grow in-Lab, Artificial media, cell culture
3. Only grow in mouse foot pad or armadillo.
4. Doubling time 14 days. Incubation period-several years
TRANSMISSION:
Prolong contact with Lepromatous leprosy
pt-
Nasal secretion, skin lesion

Organism replicate intracellularly-

Skin histocytes, Schwann cells,Endothelial cells
Cardinal Features of leprosy:★★★
● Skin lesions
● Thickened peripheral nerves
● Acid-fast bacilli on skin smears or biopsy
C/F
1)Tuberculoid Leprosy:
>CMI intact. So Lepromin skin test (+) ve.
>Hypo-pigmented lesion with thickened superficial nerve-anaesthesia
>One or few lesion with little tissue destruction.
>Number of AFB is low.

2)Lepromatous Leprosy
>CMI-poor, so lepramine test(- ) ve.
>Skin & mucous membrane lesions contain large number of organism.
>Humoral response to M. leprae intact.
>Patient is highly infections to others,

Reactions in leprosy:★★
Lepra reaction type 1 (reversal)
-Cell-mediated hypersensitivity
-Painful tender nerves, loss of function,
Swollen skin lesions, New skin lesions
Lepra reaction type 2 (erythema nodosum
leprosum)
-Immune complexe mediated
-Tender papules and nodules; may ulcerate
-Painful tender nerves, loss of function
Iritis, orchitis, myositis, lymphadenitis Fever, oedema
Lab diagnosis:
Skin lesion
Nasal Scraping
Rx
Dapsone
Rifampicin
Clofazimine
Enteric fever:★★★
>Enteric fever is caused by salmonella typhae.10^5 organism cause disease.
>Typhoid and paratyphoid fevers are transmitted by the faecal-oral route.
>The incubation period is about 10-14 days
>The temperature rises in a stepladder fashion for 4 or 5 days with malaise, increasing
headache, drowsiness and aching in the limbs.

Clinical Features of Typhoid Fever

First week
• Fever
• Headache
• Myalgia
• Constipation
• Diarrhoea and vomiting in children
.Relative bradycardia
End of 1st week
Rose spots on trunk
Abdominal distension
Splenomegaly
Diarrhoea
Cough
End of 2nd week
Delirium, complications, then coma and death (if untreated)

Complications Of Typhoid Fever:★★

Bowel
• Perforation
• Haemorrhage
Septicaemic foci
• Bone and joint infection
. Cholecystitis
. Meningitis
Toxic phenomena
• Myocarditis
. Nephritis
Chronic carriage
• Persistent gallbladder carriage

Diagnosis
a.Blood culture in 1 wk
b. Stool culture in 3rd & 4th wk
c. Urine culture in 2nd & 3rd wk
Serological test
-Widal test

Treatment
Antibiotics should be continued for 14 days
Prevention
Vaccine(both injectable & oral)

AMOEBA HISTOLYTICA:★★

Entamoeba histolytica causes amebic dysentery and liver abscess

Habitat:
Trophozoites of e. Histolytica live in the mucous and submucous layers of the large intestine
of man.
Host:
Only man. Natural infection is seen in men & monkey.

Mode of infection:
Ingestion of mature cyst.
Transmitted primarily by the fecal-oral route in
contaminated food and water. Anal-oral transmission e.g. Among male homosexuals, also
occurs.

Clinical presentations of entamoeba histolytica infection:

Asymptomatic cyst passage
Dysentery
Fulminant colitis with perforation or megacolon
Peritonitis
Perianal ulceration or other cutaneous disease
Genitourinary disease
Liver abscess
Lung abscess
Empyema
Pericarditis
Brain abscess

Hepatic amoebiasis:★★
● Located in the postero-superior surface of the right lobe of the liver.
● The trophjozoites of E. histolytica are carried as emboli by the radicles of the portal vein
from the base of an amoebic ulcer in the large intestine.
● Anaemic necrosis of the liver cells which forms the starting point of a liver abscess.
Pus of Liver Abscess:
"Pus" is not of suppuration but is a mixture of sloughed liver tissue and blood. It is chocolate
brown in colour and thick in consistency (the so-called "anchovy-sauce pus"). The smell is
rarely offensive.

Management:
Intestinal and early hepatic amoebiasis responds quickly to oral metronidazole (800 mg 8-
hourly for 5-10 days) or other long-acting nitroimidazoles like tinidazole or ornidazole (both in
doses of 2 g daily for 3 days).

Giardia intestinalis:★★
Habitat
Duodenum and the upper part of jejunum of man.
Morphology
Trophozoite: tennis or badminton racket shape. It is bilaterally symmetrical.
Cyst: infective form

Pathogenesis
>Trophozoite cause inflammation of the duodenal mucosa, leading to malabsorption of protein
and fat.
>IgA deficiency greatly predisposes to
symptomatic infection.

Clinical findings
>Watery (non bloody), foul-smelling diarrhea is accompanied by nausea, anorexia,
flatulence, and abdominal cramps persisting for weeks or months.
>There is no fever.
Laboratory diagnosis
>Diagnosis is made by finding trophozoites or cysts or both in diarrheal stools.
>string test
>No serologic test is available.
Treatment
The treatment of choice is metronidazole or quinacrine hydrochloride

Malaria:★★★
Malaria is the most common infectious disease & leading cause of death

Host-★★★
Man intermediate, female anopheles mosquito definitive host.

Characteristics of the organisms of malaria★★

>Infection of P vivax in plain land area, falciparum hilly area, Malariae subtropical area
>P vivax & ovale invades reticulocyte
>P malariae invades normoblast/mature red cells
>P falciparum invades RBC of all ages specially young RBC (> 5% RBC)
>P vivax cannot enter into red cells that lack duffy blood group
>G6PD deficiency patients are immune to malaria eg. P falciparum
>P falciparum causes high level parasitemia, profound anemia, splenomegaly, Hepatomegaly
(⅓)
>Malaria also transmitted by BT, IV drug abusers

★★Relapse by- P vivax, ovale

★★Recrudsence by- P falciparum & malariae

Clinical Findings:
● Malaria presents with abrupt onset of fever and chills, accompanied by headache,
myalgias, and arthralgias, about 2 weeks after the mosquito bite.

● Fever may be continuous early in the disease. The typical periodic cycle does not
develop for several days after onset. The fever spike, which can reach 41°C, is
frequently accompanied by shaking chills, nausea, vomiting, and abdominal pain. The
fever is followed by drenching sweats. Patients usually feel well between the febrile
episodes.

● Splenomegaly is seen in most patients, and hepatomegaly occurs in roughly one-third

● Anemia is prominent.

Laboratory Diagnosis:
● Diagnosis rests on microscopic examination of blood, using both thick and thin
giemsa-stained smears.
● The thick smear is used to screen for the presence of organisms, and the thin smear is
used for species identification.
● If more than 5% of red blood cells are parasitized, the diagnosis is usually P. falciparum
malaria.

Plasmodium Falciparum:★★
● Malaria caused by P. falciparum is more severe than that caused by other
plasmodia.
● It is characterized by infection in far more red cells than the other malarial species and
by occlusion of the capillaries with aggregates of parasitizing cells.
● This leads to life-threatening hemorrhage and necrosis, particularly in the brain
(cerebral malaria).
● Furthermore extensive hemolysis and kidney damage occur, with resulting
hemoglobinuria. The dark color of the patient's urine has given rise to the term
"blackwater fever.
Complications of falciparum malaria:
★★
● Coma (cerebral malaria)
● Hyperpyrexia, coma, paralysis.
● Spontaneous bleeding and coagulopathy
● Intravascular haemolysis
● Metabolic acidosis
● Hyperpyrexia
● Shock
● Cold and clammy skin with vascular
● collapse leading to peripheral circulatory failure.
● Hypotensive shock
● Shock secondary to septicemia
● Convulsions
● Hypoglycaemia, especially with quinine treatment

Prophylactic dose of malaria:★★

Chloroquine resistance high
Mefloquine
or Doxycycline
or Malarone
Chloroquine resistance absent
Chloroquine
proguanil

LEISHMANIA DONOVANI:★★★

> L donovani causes- Kala-azar,PKDL

> L tropica-oriental sore
> L major & mexicana-cutaneous leison
> L brazilliensis (New world)- Mucocutaneous leishmaniasis

Highlighted Point:★★
● Vector-Sand fly (carries promastigote form)★★★
● After bite promastigote taken by monocyte & RE system & converts into Amastigote form
● S/S-Hepatosplenomegaly, Lymphadenopathy, Anaemia,
● Leucopenia(Dangerous), thrombocytopenia, pyrexia, dry rough,harsh,darkened skin,
tongue moist smooth.
● Pt may die due to splenic rupture, leucopenia

★★★L. donovani is the cause of kala-azar (visceral leishmaniasis)

Laboratory Diagnosis:
a) Direct-★★
● PBF-amastigote form
● Culture (NNN media)-Promastigote form
● Biopsy-Lymph, sternal/ splenic puncture/ bone marrow study
b) Indirect-★
CBC, Aldehyde test (Positive after 3 months), CFT, ELISA, rk39 test (single best test)

★★★Promastigote form: Sand fly, Culture media

★★★Amastigote form: Human body, Buffy coat,

Treatment:
>A good response results in fever resolution, improved well-being, reduction in splenomegaly,
weight gain and recovery of blood counts.
>Recovery results in permanent immunity

According to National Guideline:

★★★1st line:
Liposomal Amphotericin B, Paromomycin,
Miltefosin
★★2nd Line:
Amphotericin B deoxycholate, Sodium
Stiboglunate

In kala-azar anaemia occurs due to:★★★

1. Bone marrow hypoplasia.
2. Haemolysis of RBC.

Clinical manifestations of PKDL:★★

1. Depigmented macules one trunk,
extremities.
2. Erythematous patches in nose, checks & chin
3. Yellowish pink nodules (painless)

Microfilaria is Produced by :★★

a) W. bancrofti
b) Brugea malayi
c) Oncocerca volvulous
d) Dracanculus medinensis

Microfilariae are not found in the peripheral blood in the following conditions:★★
1. In cases of elephantiasis,
2. After an attack of lymphangitis
3. During early allergic manifestations.
4. In occult filariasis.

RABIES VIRUS:★★★
● It is a bullet-shaped SS RNA Enveloped Virus. Infect all mammals.
● Rabies virus attaches to the acetylcholine receptor on cell surface.
● It causes viral encephalitis.
● The virus multiplies locally at the bite site & infects the sensory neurons. It moves by
axonal transport to CNS, then travels down the peripheral nerves to the salivary glands
and other glands.
● There is no viremic stage. Infected neurons contain negri body.
● Inc. Period: 9-60 days
● Transmitted by bite of infected rabid animals
● Negri Body Pathognomonic: Eosinophilic Cytoplasmic Inclusion in infected Neuron
Rx:
No antiviral therapy, only supportive Rx.

Mortality -★★★ 100%

Prevention: ★★★
● Passive active immunization.
● Vaccine: available
● Preexposure vaccine- given to high risk groups: veterinarians, zookeepers, travelers to
the area of hyperendemic zones Dose: 0,7 & 21/28th days
● Postexposure Vaccine: Dose-0, 3, 7, 14, 28 (+90 days Davidson) with 1st dose
Rabies Ig (Rig)

Available Vaccines-★★
a) Duck Embryo Vaccine (Immunogenicity low)
b) Nerve tissue vaccine-can cause an allergic encephalomyelitis due to cross reaction with
myelin sheath
c) Human diploid cell vaccine- It is preffered

Clinical Findings of rabies:★

>Fever anorexia
> changes in sensation at the bite site
>confusion lethargy
> increased salivation
> painful spasm of the throat muscles, >hydrophobia to swallowing.
HUMAN IMMUNODEFECIENCY VIRUS:★★

Important notes
Both HIV-1 and HIV-2 cause AIDS. Preferentially infects and kills helper (CD4) T
lymphocytes, resulting in loss of mediated immunity.
● A high probalility that the host will develop opportunistic infections. Other cells (e.g.
macrophages and monocytes) that have CD4 proteins on their surfaces can be infected
also.
● Contains Reverse Transcriptase enzyme (RNA dependent DNA polymerase)
● HIV genome is the most complex genome
● Structural gene- gag,pol,env

Most important opportunistic infection:★★

>Pneumocystis jirovecii pneumonia
>Kaposi's Sarcoma

Rx-HAART (Highly active anti retroviral therapy)

Transmission: ★★★
1. Sexual transmission
Vaginal intercourse: female to male, male to female
Anal intercourse: insertive, receptive
Oral intercourse: insertive, receptive
Linked commercial sex
2. Occupational transmission
Deep injury
Visible blood on device, Mucous membrane splash
3. Injection drug use transmission
Sharing equipment
Blood transfusion
Intravenous drug-users sharing needles
Percutaneous needlestick injury
4. Mother to child
Vaginal delivery
Breastfeeding

Clinical Findings:
● The three main stages of HIV infection-acute, latent, and immunodeficiency.
● Antibodies to HIV typically appear 10-14 days after infection, will have seroconverted by
3-4 weeks after infection.
Clinical features of primary infection
● Fever
● Maculopapular rash
● Pharyngitis
● Lymphadenopathy
● Myalgia/arthralgia
● Diarrhoea
● Headache
● Oral and genital ulceration
● Meningo-encephalitis
● Bell's palsy

Laboratory Diagnosis:
Definitive diagnosis is made by Western blot analysis, in which the viral proteins are
displayed.
Serology:
1)Detection of Ab against HIV serum
Particle agglutination test.
ELISA (Screening test)
Western blot (Confirmatory test)
ELISA + ve Repeat → + ve → Western blot
2)Detection of HIV antigen (p24) by polymerase chain reaction (PCR)

Cancers associated with HIV★★

1. KS(kaposi sarcoma)
2. Ca-Cx
3. NHL(Non Hodgkin lymphoma)

Dengue:★★★
● Principal vector is Aedes aegypti
● Incubation period 2-7 days

Clinical features of dengue fever:★

● Prodrome: 2 days of malaise and headache
● Acute onset: Fever, backache, arthralgias, headache, generalised pains ("break-
bone fever'), pain on eye movement,
● lacrimation, anorexia, nausea, vomiting, relative bradycardia, prostration, depression
● lymphadenopathy

Fever: Continuous or 'saddle-back', with break on 4th or 5th day and then recrudescence;
usually lasts 7-8 days.
Dengue Haemorrhagic Fever or Dengue Shock Syndrome:★★
● Occurs mainly in children. In mild forms, there is thrombocytopenia and
haemoconcentration.
● In the most severe form, after 3-4 days of fever, hypotension and circulatory failure
develop with pleural effusions, ascites, hypoalbuminaemia and features of acute
respiratory distress syndrome (ARDS)
● Minor (petechiae, ecchymoses, epistaxis) or major (gastrointestinal or cerebrovascular)
haemorrhagic signs may occur.

Investigation★★
• 1st 3 days : Dengue NSI Antigen
• 3rd to 7th days : Anti dengue IgM
• After 7th days. Anti dengue IgG
Any time: RT PCR (confirmatory)

Management and prevention: ★★

● Treatment is symptomatic.
● Aspirin should be avoided due to bleeding risk.
● Volume replacement and blood transfusions may be indicated in patients with shock.
With intensive care support, mortality rates are 1% or less.
● Corticosteroids have not been shown to help.
● No existing antivirals are effective.
● There is no licensed vaccine available.

Follow-up
a) Regular BP monitoring
b) Daily CBC monitoring
i. Hematocrit
ii. Platelet

Dengue with warniMeasles

s★★
Probable dengue plus one of:
● Abdominal pain or tenderness
● Persistent vomiting
● Signs of fluid accumulation, e.g.
pleural effusion or ascites
● Mucosal bleed
● Hepatomegaly > 2 cm
● Rapid increase in haematocrit with fall in platelet count
● Needs medical intervention,IV fluid.

Virus Causing Congenital

anomaly :★★★
CMV
Rubella
HIV
HBV
HSV
Parovo-virus-B19
Measles

Virus Having Carrier

State:★★
HBV
HCV
Rubella
CMV

Transplacental Transmission of
Virus-★★★
HIV
HBV
CMV
Rubella
Parvo Virus-B19