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Ischemic colitis

  • Common in old age (90% of cases above 60 years old)
  • With previous history of polycythemia, DVT, endocarditis, atherosclerosis, AF, digoxin, danazole, gold, oestrogen, volvolous, strangulated intestinal hernia, vasculitis, systemic circulatory insufficiency, trauma, hypovolemia, sepsis, congestive heart failure, recent myocardial infarction, arrhythmias, after cardiac surgery or dialysis or radiation.
  • Acute ischemic colitis caused mainly by mesenteric thrombosis and chronic by atherosclerosis.
  • Divided to Occlusive ischemia and Non-occlusive ischemia– acute and chronic.

 

Clinical picture of ischemic colitis :

  • Pain out of proportion to exam (20% to 30% are painless). The pain is usually postprandial because of the increased blood flow required for digestion. Decreased or absent bowel sounds. Occult blood that rapidly progresses to frankly bloody stool. Hypotension, tachycardia, fever, elevated WBC count, and lactic acidosis may occur if transmural infarction occurs and peritonitis develops.
  • Intestinal perforation as a common complication.

 

Investigations:

Doppler ultrasounds, CT angiography or magnetic resonance angiography “Portal venous gas or pneumatosis intestinalis is diagnostic”. Colonoscopy.

jrodes10 Ischemic colitis

Case report 1 Mar 2005 fig2 Ischemic colitis

pandora fig4 Ischemic colitis

  Ischemic colitis

Management:

  • Conservative treatment: intravenous fluid, bowel rest, and broad-spectrum antibiotics helpeful in non-complicated cases.
  • In acute Ischemia: Surgical revascularization, percutaneous angiography guided revascularization, intra-arterial infusion of thrombolytic or vasodilator agents, or systemic anticoagulation.
  •  In chronic ischemia: Percutaneous transluminal angioplasty or arterial bypass or endarterectomy.

 

More: Ischemic colitis

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Dermatological disorders with malignancy

      1.      Acanthosis nigricans: Gastrointestinal Cancer

     m h photo of acanthosis nigricans Dermatological disorders with malignancy

 

 

2.      Acquired hypertrichosis lanuginosa: Gastrointestinal And Lung Cancer

lanuginosa2 s Dermatological disorders with malignancy

 

 

3.      Acquired ichthyosis: Lymphoma

2007111625429198 Dermatological disorders with malignancy

 

 

4.      Dermatomyositis: Bronchial And Breast Cancer

1866 Dermatological disorders with malignancy

 

 

5.      Erythema gyratum repens: Lung Cancer

eac1 s Dermatological disorders with malignancy

 

 

6.      Erythroderma: Lymphoma

M 06 Dermatological disorders with malignancy

 

 

7.      Migratory thrombophlebitis: Pancreatic Cancer

335 1 hlight Dermatological disorders with malignancy

 

 

8.      Necrolytic migratory erythema: Glucagonoma

 Dermatological disorders with malignancy

 

 

9.      Pyoderma gangrenosum: Myeloproliferative Disorders

 Crohnie Pyoderma gangrenosum Dermatological disorders with malignancy

 

 

10.  Sweet's syndrome: Haematological Malignancy, RA, IBD

 041602 7a Dermatological disorders with malignancy

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Hypokalaemia

 Hypokalaemia with acidosis (the role)

• Diarrhoea "GIT"

• Renal tubular acidosis, Acetazolamide  "Renal"

• Partially treated diabetic ketoacidosis "endocrinal"

 

Hypokalaemia with alkalosis (the exception)

• Vomiting "GIT"

• Diuretics "Renal"

• Cushing's syndrome, Conn's syndrome (primary hyperaldosteronism)  "endocrinal"

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METABOLIC ALKALOSIS

 

CHLORIDE-RESPONSIVE METABOLIC ALKALOSIS

1.     Vomiting.

2.     Nasogastric (NG) suction.

3.     Stool losses (laxative abuse, cystic fibrosis, villous adenoma).

4.     High alkali intake.

5.     Diuretics.

6.     Post-hyperventilation alkalosis.

7.     Massive blood transfusion

 

CHLORIDE-RESISTANT METABOLIC ALKALOSIS

1.     Hyperadrenocorticoid diseases (Cushing's syndrome, Conn's, 2ry mineralocorticoidism as cirrhosis of the liver and congestive heart failure ).

2.     licorice, tobacco chewing

3.     Hypomagnesemia.

4.     Hypokalemia.

5.     Bartter's syndrome: *Bartter's syndrome is an autosomal recessive disease of severe hypokalaemia due to defective chloride absorption at the Na+ K+ 2Cl cotransporter in the ascending loop of Henle. It is associated with normotension, unlike other endocrine causes of hypokalaemia such as Conn's, Cushing's and Liddle's syndrome which are associated with hypertension.

 

button METABOLIC ALKALOSIS

METABOLIC ACIDOSIS

METABOLIC ACIDOSIS WITH INCREASED anion gap (AG ACIDOSIS)

  1. Lactic acidosis.

  2. Ketoacidosis (diabetes mellitus, alcoholic ketoacidosis).

  3. Uremia (chronic renal failure).

  4. Ingestion of toxins (paraldehyde, methanol, salicylate, ethylene glycol).

  5. High-fat diet (mild acidosis).

 

METABOLIC ACIDOSIS WITH NORMAL anion gap (HYPERCHLOREMIC ACIDOSIS)

  1. Renal tubular acidosis (including acidosis of aldosterone deficiency).

  2. Intestinal loss of HCO3- (diarrhea, pancreatic fistula).

  3. Carbonic anhydrase inhibitors (e.g., acetazolamide).

  4. Dilutional acidosis (as a result of rapid infusion of bicarbonate-free isotonic saline).

  5. Ingestion of exogenous acids (ammonium chloride, methionine, cystine, calcium chloride).

  6. Ileostomy.

  7. Ureterosigmoidostomy.

  8. Drugs: amiloride, triamterene, spironolactone, β-blockers

Anion gap can be calculated by: (Na+ + K+) – (Cl- + HCO-3). 

The normal range = 10-18 mmol/L

button METABOLIC ACIDOSIS

Hepatitis B, D

 

  • Hepatitis B

  • is caused by a double-stranded DNA virus that is transmitted by parenteral exposure to infected blood, usually through skin punctures by contaminated needles. risk factors for hepatitis B infection include sexual contact and the sharing of toothbrushes and razors with an infected person; vertical transmission at birth from mother to child is also common. The hepatitis B virus is present in the blood approximately 2 months after infection, incubation period 10-15 weeks with symptoms appearing at approximately 3 months. IgM anti-HBc appears early in the disease and its measurement is the best single serologic test to confirm acute viral hepatitis B.

  • The clinical course may progress to fulminant hepatic failure and death in up to 2% of the patients, or the infection may go to a chronic carrier state in 5-10% of the patients.

  • Chronic carriers are at high risk for early death from cirrhosis or hepatocellular carcinoma and should be considered candidates for treatment with agents aimed at suppressing hepatitis B replication, as, Alpha-interferon and lamivudine.
  • Immunization with a recombinant HBsAg is highly effective and give long-term protection against infection.
  • Complications of hepatitis B: chronic infection (5-10%),  fulminant liver failure (1%), hepatocellular carcinoma, glomerulonephritis, polyarteritis nodosa, cryoglobulinaemia.
  • Serology of hepatitis B: previous immunisation: anti-HBs positive, all other markers are negative – previous hepatitis B and not a carrier: anti-HBc positive, HBsAg negative – previous hepatitis B, now is a carrier: anti-HBc positive, HBsAg positive.
  • HbeAg results from breakdown of core antigen from infected liver cells as is therefore a marker of infectivity


 

  • Hepatitis D

  • is caused by a defective RNA virus that requires the presence of HBsAg for expression. Hence, infection with the hepatitis D virus occurs only as a coinfection with hepatitis B virus, or as a superinfection in those who are chronic hepatitis B virus carriers.

  • The symptoms of hepatitis D are usually more severe than those seen with acute hepatitis B, with progression to fulminant hepatic failure and death in up to 20% of the patients. The specific serologic test for hepatitis D, anti-HD, should be carried out only if the HBsAg serology is positive.
  • There is no vaccine specific to the hepatitis D virus, although immunization against hepatitis B confers protection against hepatitis D.
button Hepatitis B, D

Hepatitis C

 • Hepatitis C is caused by an RNA virus that, like the hepatitis B virus, transmitted primarily by parenteral exposure to infected blood. • Risk of transmission during a needle stick injury is about 2% • The risk of transmitting the virus during sexual intercourse is probably less than 5% • The vertical transmission rate from mother to child is about 6% • Breast feeding is not contraindicated in mothers with hepatitis C •

Symptoms of acute infection are often mild. • 85% of infected people become chronic carriers. Such persons are at high risk for chronic hepatitis, cirrhosis, cryoglobulinaemia and hepatocellular carcinoma.

Patients with chronic hepatitis C should be considered candidates for treatment with alpha-1 interferon or the combination of interferon and ribavirin. Serologic tests for hepatitis C continue to be improved as our knowledge of the virus increases. There is no known protective antibody and no known vaccine. •

Interferon alpha – side-effects: flu-like symptoms, depression, fatigue, leukopenia, thrombocytopenia. •

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Hepatitis A, E

Hepatitis A

 

·         Commonest cause of infectious hepatitis.

·         HAV is an RNA picornavirus.

·         Transmitted via the feco-oral route, person-to-person contact or ingestion of contaminated food “ex. Uncooked shellfish”

·         Incubation period = 30 days.

·         The virus is detectable in stool from 2 weeks before and week after jaundice.

·         Endemic in Russia, Africa, Eastern Europe, Middle East, parts of South America.

·         Symptoms: flulike illness, malaise, anorexia, weakness, fever, RUQ pain, jaundice, and pruritus.  

·         Children are typically asymptomatic, smokers tend to lose interest in smoking.

·         When jaundice develops, it resolves within 2 weeks in 85%.

·         Signs: Tender hepatomegaly, splenomegaly, rash, and lymphadenopathy.

·         <10% of patients develop a relapsing course of prolonged cholestasis.  Especially in patients with sickle cell anemia .

·         Extrahepatic manifestations: auto-immune glomerulonephritis, vasculitis,

·         Mortality rate is 1% in patients over the age of 40 years.

·         Severe form of disease occurs in  pregnancy or in patients has liver disease. 

·         ALT/AST are elevated in first 2 months.

·         PCR can detect viral antigens.

·         Detection of immunoglobulin (Ig) M anti-HAV antibody confirm diagnosis, IgG  means resolved immunity from prior infection or vaccination.

·         Liver biopsy can show focal necrosis with periportal inflammation.

·         Management is supportive with symptomatic treatment.

·         Bed rest does not accelerate recovery and early ambulation should be encouraged.

·         Hospitalization of patient with severe or persistent anorexia, encephalopathy, or coagulopathy.

·         Corticosteroid therapy may be useful in accelerating resolution of the prolonged cholestatic phase.

·         Prevention of infection is possible via passive immunization and vaccination.

·         Passive immunization is the method of choice for post-exposure prophylaxis because immunity develops within 3 to 5 days and lasts up to 3 months.

·         The inactivated vaccine gives immunity for at least 5 to 10 years and consists of a sequence of two or three injections.

 

 

 

 

 

Hepatitis E

 

 

·         The incubation period about 40 days.

·         Transmitted in a faeco oral route (similar to hepatitis A).

·         Hepatitis E is usually a self-limiting infection followed by complete recovery and there is no chronic infection, prolonged viraemia or faecal shedding is rare.

·         A fulminant form of hepatitis E can develop, especially in pregnancy and with a mortality rate of 20% in the third trimester.

·         The condition should therefore be suspected in outbreaks of water-borne hepatitis occurring in developing countries, especially if the disease is more severe in pregnant women, or if hepatitis A has been excluded.

·         Diagnosis can by testing for the presence of specific viral antigens and/or antiviral antibodies “IgM or IgG”.

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Coeliac Disease

Coeliac disease is the most common cause of malabsorption syndrome in western world” Prevalence of coeliac disease is estimated to be as high as 1 in 200 in the Western world” which caused by sensitivity to the protein gluten which present in all foods made from wheat, barley or rye and probably oats except: rice, potatoes and corn (maize). IgA antibodies to gliadin are commonly positive in the serum of patients. Serum anti-endomyseal antibody and anti-tissue transglutaminase antibodies are more specific. Repeated exposure leads to villous atrophy which in turn causes malabsorption. About 35% of patients present in the childhood, but it can occur in any age. Mode of presentation is variable with very subtle (failure to thrive, growth retardation or anaemia) or more obvious with fatty diarrhoea and feature of malabsorption.Conditions associated with coeliac disease include dermatitis herpetiformis (a symmetrical vesicular, pruritic skin eruption and IgA deposits are found at dermo-epidermal junction) and autoimmune disorders (type 1 diabetes mellitus and autoimmune hepatitis). It is strongly associated with HLA-DQ2 (95% of patients) and HLA-B8 (80%) as well as HLA-DR3 and HLA-DR7.

The management of coeliac disease is a gluten-free diet   


 

Classical case of Coeliac Disease

           A 38-year-old man presents with a 8-month history of abdominal bloating, diarrhoea, bone pain, and an itchy vesicles over the extensor surfaces of the forearm . he complains recently from difficulty getting out of his chair. On examination, he has palor with multiple bruises and a symmetrical vesicular rash over his forearms, buttocks and knees.Investigations: Hb: 8.5. WBC: 3.6. Plts: 101. MCV: 97 Blood film: Microcytes, macrocytes, hypersegemented neutrophils and Howell- Jolly bodies.

 

 Complications of Coeliac Disease

·       Anaemia: iron, folate and vitamin B12 deficiency (folate deficiency is more common than vitamin B12 deficiency in coeliac disease)

·      Hyposplenism

·      Lactose intolerance

·      80-fold increase in small bowel carcinoma

·      Oesophageal cancer, other malignancies

·      Collagenous sprue – excessive subepithelial collagen deposition.

·      Lymphocytic gastritis is  a dense epithelial lymphocytic infiltration

·      About 10% of patients with coeliac disease have an isolated immunoglobulin A (IgA) deficiency

·      Associated with chronic liver disease, inflammatory bowel disease, diabetes melliteus, thyroid disease, addison's disease, fibrosing alveolitis, systemic lupus erythematosus, polyarteritis nodosa and temporal lobe epilepsy  

 

 Another case of Coeliac Disease

A 25-year-old woman complains of an itchy symmetrical rash over his arms, tiredness, recurrent abdominal pain and intermittent diarrhoea with a 11-kg weight loss over six months. She is pale and has a rash on her elbows and knees. Laboratory data shows a microcytic, hypochromic anaemia and low folate and ferritin levels, a low serum albumin and slightly raised TSH level and normal free T4.   

button Coeliac Disease

Causes of Chronic Liver Disease

 


 

·         Alcohol

·         Paracetamole

·         Amiodarone

·         Isoniazid

·         Arsenic

·         Nitrofurantoin

·         Propylthiouracil

·         Vinyl chloride

 

·         Hepatitis B and C

·         CMV

 

·         Tuberculosis

·         secondary syphilis

·         Fungal

·         Sarcoidosis

 

·         Primary biliary cirrhosis

·         Primary sclerosing cholangitis

·         Autoimmune chronic hepatitis

 

·         Wilson's disease

·         Hemochromatosis

·         Glycogen storage disease

·         Gaucher's disease

·         Alpha 1-Antitrypsin deficiency

 

button Causes of Chronic Liver Disease

Crohn’s Disease and Ulcerative Colitis

 

Crohn's Disease and Ulcerative Colitis

 

Crohn's Disease

Ulcerative Colitis

Pathologic features

 

 

Transmural inflammation

Deep ulcers

Granulomas common “non caseating”

Mucosal inflammation

Superficial ulcers

Granulomas absent

Site

Mouth to anus

(ileum and proximal colon most common)

Colon

Ileal involvement

Narrowed lumen with thickened wall

Dilated lumen & diminished folds.

Rectal involvement

Up to 50%

More than 95%

Rectal bleeding

Less than 40%

More than 90%

Fulminating attacks

Uncommon

Common

Obstruction

Common

Rare

Fistulas

Common

Rare

Perianal disease

Common

Less common

Extent

Patchy

Continuous

Ulcers

Deep,longitudinal

Shallow, button like

Pseudopolyps

Uncommon

Common

Strictures

Common

Uncommon

 

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Foramina of the skull

Summary of important foramina

foramen  

vessels  

nerves  

foramina of cribriform plate

-

olfactory nerve bundles (I)

optic canal

ophthalmic artery

optic nerve (II)

superior orbital fissure

superior ophthalmic vein
inferior ophthalmic vein

oculomotor nerve (III)
trochlear nerve (IV)
lacrimal, frontal and nasociliary branches of ophthalmic nerve (V1)
abducent nerve (VI)

foramen rotundum

-

maxillary nerve (V2)

inferior orbital fissure

inferior ophthalmic veins
infraorbital artery
infraorbital vein

zygomatic nerve and infraorbital nerve of maxillary nerve (V2)
orbital branches of pterygopalatine ganglion

foramen ovale

accessory meningeal artery

mandibular nerve (V3)
lesser petrosal nerve (occasionally)

foramen lacerum
(or carotid canal)

internal carotid artery

internal carotid nerve plexus

internal acoustic meatus

labyrinthine artery

facial nerve (VII)
vestibulocochlear nerve (VIII)

stylomastoid foramen

stylomastoid artery

facial nerve

jugular foramen

posterior meningeal artery
ascending pharyngeal artery
inferior petrosal sinus
sigmoid sinus
internal jugular vein

glossopharyngeal nerve (IX)
vagus nerve (X)
accessory nerve (XI)

hypoglossal canal

-

hypoglossal nerve (XII)

foramen magnum

vertebral arteries
meningeal branches of vertebral arteries

medulla oblongata
spinal roots of accessory nerves

Read more details about the Foramina of the skull on Wikipedia: http://en.wikipedia.org/wiki/Foramina_of_skull

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Autoantibodies

Read more about Autoantibodies on wikipedia:

Click HERE to take this test:

 

Spectrum Autoantibodies

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Drugs unsafe in acute porphyria (AIP)

Bacteriostatic and Bacteriocidal Antibiotics

Bacteriostatic Antibiotics

Others are Bacteriocidal.

Read more: http://knol.google.com/k/amol-kothalkar/antibiotics

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