Massive splenomegaly common causes

* Chronic myeloid leukaemia
* Myelofibrosis
* Lymphoma
* Thalassaemia major or intermedia
* Gaucher's disease
* Leishmaniasis
* Tropical splenomegaly

To remember reflexes and the nerves

• One, two, buckle my shoe - ankle jerk : S1-2
• Three, four, kick at the door - patellar tendon : L3-4
• Five, six, pick up sticks - biceps/brachioradialis : C5-6
• Seven, eight, close the gate - triceps: C7-8

How Angiotensin Converting Enzyme (ACE) Inhibitors cause increase in bradykinin

• Angiotensin Converting Enzyme (ACE) degrades bradykinin, not only converting angiotensin I to angiotensin II
• So, when ACE inhibitors present, bradykinin is not broken down
• There will be high level of bradykinin
• Causing side effect such as chronic dry cough

Diabetes type I (insulin dependent), beta-blockers and hypoglycemia

• Diabetes type I patients could not produce enough insulin due to destruction of beta-cells in Pancrease that produce insulin.
• These patients will get hyperglycemia (high blood glucose) if they do not take insulin.

• So, they will take insulin, to control the level of glucose.
• The level of glucose in the blood will decrease by doing that.

• Beta-blockers stimulate release of insulin from the remaining beta-cells.

• When these patients take beta-blockers and insulin at the same time, there will be over dose of insulin (own insulin + artificial insulin)
• Patient will get hypoglycemia (low blood glucose)

• Worse, beta-blockers ‘mask’ the hypoglycemic signs such as tremor and palpitation.
• The unlucky patient and the doctors wouldn’t notice that there is hypoglycemia going on.

• If left untreated, patient will die due to hypoglycemia.

Drugs to cure rheumatoid arthritis

These are some of the drug concepts scientists are using to find the cure for rheumatoid arthritis. I wish them all the best to find the cure!

TNF-alpha inhibitors
Tumor necrosis factor-alpha causes inflammation. By blocking the the protein, it will reduce and control the inflammation.

Interleukin-6 (IL-6) inhibitor
This protein causes inflammation with TNF-alpha, though it isn't clear how.

Interleukin-15 (IL-15) inhibitor
This protein activates inflammatory processes in the lining that surrounds your joints (synovium). People with rheumatoid arthritis have high levels of IL-15

Drugs that stop B cells from causing inflammation
B cells cause joint inflammation in people with rheumatoid arthritis

Differences between Crohn’s Disease with Ulcerative Colitis

Crohn’s disease:

• affecting colon and ileum
• affecting mucosa, submucosa and muscularis
• skip lesion distribution
• deep linear ulcers
• granulomas present (50%)
• fistula present
• there are fat and vitamins malabsorption
• responses to surgery is poor

Ulcerative colitis

• affecting colon
• affecting mucosa and submucosa
• diffuse distribution
• superficial ulcers
• no granuloma
• no fistula
• no fat and vitamins malabsorption
• response to surgery is good

Bowel sound and mechanical bowel obstruction

• Mechanical bowel obstruction causes proximal part to the obstructed area to distend.
• This compromises blood flow
• Causing venous obstruction
• Which leads to shortage of arterial supply
• Ischemia happens and leads to infarct
• Infarction means no peristalsis
• No peristalsis, no bowel sound

Smoking and peptic ulcer

Smoking impairs blood flow to mucosa. Impairs healing process. Leads to or worsen the ulcer.

Pathophysiology of colicky pain

• obstruction / blockage of a tube
• increase in peristalsis in order to remove the cause of ibstruction
• leads to vigorous muscular contraction
• cause ischemia
• lactic acid accumulation and spasm
• irritate nerve endings
• pain

Hepatorenal syndrome (HRS)

Definitions

Renal failure
- situation in which the kidneys fail to function adequately

Hepatorenal syndrome
- acute renal failure
- that occurs in the setting of cirrhosis or fulminant liver failure
- sometimes also associated with portal hypertension
- usually in the absence of other disease of the kidney

Pathophysiology

2 Theories

1.

• cirrhosis or fulminant liver failure
• cause portal hypertension
• renal perfusion is maintained by vasodilatory systems
• as liver disease progresses in severity, renal vasodilatory systems are unable to counteract the maximal activation of the endogenous vasoconstrictors and/or intrarenal vasoconstrictors
• leads to uncontrolled renal vasoconstriction.

2.
- unrelated to systemic hemodynamics but is due to either a

• deficiency in the synthesis of a vasodilatory factor OR
• hepatorenal reflex that leads to renal vasoconstriction.

Coombs’ test

What is this test for?
Looks for antibodies that act against your red blood cells.

Types
Direct antiglobulin test; Indirect antiglobulin test

Direct Coombs test

The Concept

• IgG antibodies that specifically bind to antigens on the red blood cell (RBC) surface membrane
• Red blood cells (RBCs) become coated with IgG alloantibodies (an antibody that occurs naturally against foreign tissues from a person of the same species) and/or IgG autoantibodies (An antibody that reacts with the cells, tissues, or native proteins of the individual in which it is produced)
• Complement proteins may subsequently bind to the bound antibodies

So,
- Coombs test is used to detect these antibodies or complement protein
- Red blood cells are taken
- Coombs reagent (antihuman globulin) incubated with the red blood cells
- if there are antibodies or complement proteins bound to red blood cells, agglutination occurs

Indirect Coombs test
- Used in pregnant women, and to test blood in blood tranfusion
- Detects antibodies which are not bound to red blood cells of patients
- If agglutination occurs, the indirect Coombs test is positive.
- rarely used to diagnose a medical condition


Examples

Alloimmune hemolysis

o Rhesus hemolytic diseases of the newborn
o Systemic lupus erythematosus
o Evans' syndrome (antiplatelet antibodies and hemolytic antibodies)
o Etc

Drug-induced immune-mediated hemolysis

o Methyldopa (IgG mediated type II hypersensitivity)
o Penicillin (high dose)
o Quinidine
o Etc

Antistreptolysin O titer (ASOT)

• Group A streptococci produce the enzyme streptolysin O, which can destroy red blood cells.
• Body reacts by producing antistreptolysin O to neutralize it.
• A high titer indicates there isor has been a streptococcal infection or has been present.
• ASO appears in the blood serum one week to one month after the onset of a strep infection.
• Normal value : < 200 Todd units
  

Titer : standard of strength of a volumetric test solution; the assay value of an unknown measure by volumetric means

Jones criteria for Rheumatic Fever (mnemonics included)

Major criteria

Joints : polyarthritis
O : heart-shaped O due to carditis
Nodules : subcutaneous nodules
Erythema marginatum
Sydenham's chorea (St. Vitus' dance)

OR

C : Carditis
A : Arthritis, poly
N : Nodules, subcutaneous
C : Chorea, Sydenham's
ER : ERythema Marginatum

Minor Criteria

- Fever
- Arthralgia (joint pain without swelling)
- Laboratory abnormalities:

increased Erythrocyte sedimentation rate,

increased C reactive protein,

leukocytosis

- prolonged PR interval
- elevated or rising Antistreptolysin O titre, or DNAase (evidence of Group A Strep infection)
- previous rheumatic fever or inactive heart disease

Don't get confused with rheumatic fever with rheumatic heart disease

Rheumatic fever
inflammatory disease
which may develop after a Group A streptococcal infection

Rheumatic heart disease
disease of the heart resulting from rheumatic fever

Acute VS Chronic Heart Failure Presentations

Acute heart failure

• severe dyspnoea
• orthopnea
• fronthy pinkish sputum (pulmonary oedema)
• hypotension
• pallor
• cyanosis

Chronic heart failure

• reduce exercise tolerance
• fatique
• exertional dyspnoea
• peripheral oedema
• JVP distension
• hepatomegaly
• serous effusion

Is reperfusion after myocardial infarction beneficial to all patients?

Myocardial reperfusion may not benefit all patients and may actually be harmful to some. Components of reperfusion injury may occur not only in isolation but also in combination--when more profound consequences might be expected. The exact mechanisms of reperfusion injury are uncertain, but they probably include cellular overload of calcium, osmotic cell swelling, and myocyte or microvascular damage from cytotoxic free radicals derived from oxygen

http://www.bmj.com/cgi/content/full/310/6978/477

Although reperfusion is essential for salvage of the ischemic heart, reperfusion beyond a certain period of ischemia may cause injury to the myocardium. Dramatic changes in contractile function, arrhythmias, and ultrastructure occur in the ischemic-reperfused heart as a consequence of the generation of oxyradicals, loss of cation homeostasis, depletion of energy stores, and changes in subcellular activities. These acute effects of reperfusion appear to be the result of the occurrence of oxidative stress and intracellular Calcium overload in the heart. Alterations in cardiac gene expression may account for delayed recovery of subcellular organelles in the ischemic myocardium.

http://www.heartandmetabolism.org/pdf/37/8.pdf

Necrotizing arteriolitis and malignant hypertension

necrotizing arteriolitis
- necrosis in the media of arterioles
- characteristic of malignant hypertension

malignant hypertension
- a complication of hypertension
- characterized by

• very elevated blood pressure (usually greater than 220/120)
• organ damage in the eyes, brain, lung and/or kidneys

MacConkey agar / McConkey agar concept

What is this for?
designed to grow Gram-negative bacteria and stain them for lactose fermentation.
distinguishes those Gram-negative bacteria that can ferment the sugar lactose from those that cannot

Contents
It contains :

• bile salts and crystal violet dye to inhibit most Gram-positive bacteria
• neutral red dye to stains microbes fermenting lactose
• lactose and peptone.

The concept :

• bacteria that can ferment sugar lactose will produce acid
• lowers the pH
• appearance of red/pink colonies.

• bacteria that cannot ferment sugar lactose will use peptone
• producing ammonia
• raise pH
• appearance of white / colourless colonies

Macconkey agar with lactose (left) and non-lactose (right) fermenters

Why do we use Ziehl-Neelsen stain, not gram stain for mycobacterium tuberculosis?

Ziehl-Neelsen stain, also known as the acid-fast stain, is a special bacteriological stain used to identify acid-fast organisms, mainly Mycobacteria. Acid fast bacteria are stained bright red and other organism and background will be blue. Acid-fast bacteria are bacteria that resistance to decolorization by acids during staining procedures.

Why do we use Ziehl-Neelsen stain, not gram stain?
Acid fast bacteria cell walls contain peptidoglycan but they have a waxy coat on their cell wall too. Gram stain (crystal violet nor the counterstain (safranin)) can not penetrate the waxy layer. Therefore they will not be visible able to see under the microscrope.

Per-rectal examination and prostate enlargement characteristics

Benign (nonmalignant character of a neoplasm) enlargment
- smooth and firm

Prostatic carcinoma
- hard and irregular