+ 250 100
- 750 900
Sensitivity= 250/1000= 0.25
Specificity= 900/1000= 0.9
Disease prevalence= 10% , this means that 10,000 people have the disease
90,000 do NOT have disease
Sensitivity = 25%, so 25% will be diagnosed correctly..... so TP = 250
Specifity= 90%... so there are 90,000 x 0.9 TN's = 81,000
Next, fill in the rest.
+ 2,500 9,000
- 7,500 81,000
Systemic mastocytosis, often termed systemic mast cell disease (SMCD), is a myeloproliferative neoplasm characterized by infiltration of clonally derived mast cells in different tissues, including bone marrow (see the image below), skin, the gastrointestinal tract, the liver, and the spleen.
The mast cells secrete excess histamine. Histamine in turn, causes gastric hypersecretion.
Because gastric acid secretion increases, this inactivates pancreatic and intestinal enzymes, causing diarrhea.
Often also presents with histamine mediated symptoms:
Skin manifestations (pruitis, urticarial)
Dementia is memory loss, cognitive dysfunction, but NO loss is consciousness
- Slow-onset memory loss (takes years to develop, begins with recent memories, progesses to long term memories)
- progressive disorientation, forget daily tasks
- Lose motor and language skills
- Behavior/personality changes (ie, apathy, anger)
Patients eventually become mute and bedridden.
Important to note that we do not get focal neurologic deficits early in the disease (pill rolling tremor, expressionless face, choria, etc etc)
Diffuse cerebral atrophy of the brain.
Atrophy is hallmarked by narrowing of the gyri, and widening of the sulci
As a consequence of atrophy, the ventricles dilate and take up the space, and this is called hydrocephalus ex vacuo.
Development of neuritic plaques, full of A-beta Amyloid which is extracellular which entraps neurotic processes
Note: A-beta Amyloid can also deposit around the cerebral vessels of the brain, and this is called cerebral Amyloid angiopathy , which weakens the wall of the vessels and increases risk of hemorrhage !!!
Formation of neurofibrillary tangles, which includes the Tau protein, which helps organize the microtulules... here, the Tau is hyperphosphorylated and thus can no longer assist in organizing microtubules, so they become tangled
Normally signs of hypoglycemia include
1) neurogenic ones from excess catecholamines (initial)- sweating, diaphoresis, hunger, tingling, tremor, palpitations, chest pain, anxiety. .... These are BLOCKED by NON-selective beta blockers!!!! Blocked because beta blockers (especially non-selective ones with B2 antagonists) block the catecholamine response.
neuroglycopenic ones from lack of glucose (happens later)- weakness, confusion, drowsiness, dizziness, syncope, blurred vision.
#metabolic acidosis and anion gap
# causes of increased Anion gap acidosis
• Uremia - advanced, chronic renal failure
• Diabetic ketoacidosis (β-hydroxybutyrate, acetoacetate)
• Phenformin, Paraldehyde
• Iron, Isoniazid
• Lactic acidosis - from shock, hypoxia, exercise, poor tissue perfusion, enzyme deficicncies etc.
• Ethanol, Ethylene glycol
• Salicylates - with concomitant respiratory alkalosis
#Examples of normal anion gap acidosis include
• Fistula (small bowel, pancreatic) - loss of HCO3-
• Ureterogastric conduits (i.e. urine-diverting colostomy) - loss of HCO3-
• Saline administration - gain of Cl-
• Endocrine (i.e. hyperparathyroidism - a cause of type 2 renal tubular acidosis, Addison's disease - aldosterone deficiency)
• Diarrhea - loss of HCO3-
• Carbonic anhydrase inhibitors (i.e. acetazolamide - most common cause of type 2 renal tubular acidosis in adults) - loss of HCO3-
• Acid infusion (i.e. NH4Cl, hyperalimentation with total parenteral nutrition if arginine HCl or lysine HCl are used as amino acids) - gain of Cl-
• Renal tubular acidosis
• Spironolactone administration
malnutrition with inadequate protein ONLY (adequate carbohydrates, calories)
• The typical presentation of kwashiorkor is a child with a swollen belly due to ascites (accumulation of fluid in the peritoneal cavity) and an enlarged, fatty liver. Patients may also have normal or near normal height and weight, anasarca, pitting edema of the lower extremities, dry, atrophic, peeling skin, dry hair that falls out easily, and dilated intestinal loops.
• In some areas, kwashiorkor presents between ages 1-3 when a child that received enough protein while breastfeeding is displaced by a new child.
• Decreased protein consumption leads to decreased protein production. Because of the decreased protein production the capillary oncotic pressure decreases and this leads to tissue edema in kwashiorkor. The following mnemonic might be useful: You need water to wash → kwashiorkor has excess water (edema).
• The fatty liver in kwashiorkor is due to decreased apolipoprotein synthesis. Because of decreased apolipoprotein synthesis, fats that would be exported from the liver by apolipoproteins are trapped.
"An autosomal recessive defect in CFTR, a transmembrane ATP chloride channel on chromosome 7 (usually a deletion of Phe 508) !!!! The mutation causes a misfolded protein and the protein is retained in the RER instead of transported to the cell membrane!!!
In respiratory and epithelium exocrine glands, normal CFTR allows active luman sodium chloride secretion... while mutated CFTR causes DECREASED CHLORIDE SECRETION so there is HIGH levels of chloride intracellularly, and thus, INCREASED SOCIUM and H2O REABSORPTION . results in thickened DEHYDRATED MUCUS secretions, severely affecting function of the pancreatic, pulmonary, and reproductive systems, causing mucus plugs.
In sweat glands, normal CFTR reabsorbs chloride, and enhances socium reabsorption. While mutated CFTR diminishes sodium chloride reabsorption and thus, increases sweat tonicity. So, we sweat out a ton of NaCl.
Ataxia, memory impairment/confusion, nausea/vomiting, course hand tremors.
Can progress to ataxia, incoordination, hyperreflexia, blurred vision as it worsens..... can eventually progress to seizures/coma.
edema, weight gain (causes hypothyroidism),
- nephrogenic diabetes insipidus (causes polyuria, inability to concentrate urine), (!!!) It acts as ADH antagonist!!!!
→ requires monitoring of kidney function (GFR) and thyroid function (TSH levels)
• Requires a close monitoring of serum levels due to narrow therapeutic range and toxic levels can cause altered mental status, convulsions, and death
They occur due to dopamine D2 blockade, which removes dopamine's inhibitory ability, and allows excess M1 cholinergic actibity
The 4 extrapyramidal symptoms (EPS) occur in 4's:
4 hours → Acute dystonia: sudden onset sustained involuntary PAINFUL contractionn*.... of neck/muscles, tongue and oculogyric crisis (forced elevation of the eyelids!!!!)
treat with antihistamines or anticholinergics !!!!
4 days → Akathisia: subjective anxiety and restlessness, nervousness, causes person to be objective fidgetiness . .... fidgeting like a cat!!!!*... Akathisia: treated with propranolol (non-selective beta blocker)
4 weeks → Akinesia: Parkinsonian symptoms (masklike face, cogwheel rigidity, pill-rolling tremor
4 months → Tardive dyskinesia: choreoathetoid (writhing) involuntary movements of mouth and tongue (biting, chewing, grimacing, tounge protrusions).
Acute dystonia and akinesia due to unopposed cholinergic action:
treated with anticholinergics (benztropine or trihexyphenidyl) !!!
Perhaps the most feared complication of typical antipsychotics is an idiosyncratic reaction characterized by severe muscle rigidity, hyperreflexia, myoglobinuria and elevated plasma creatine kinase, fever/hyperthermia, autonomic instability, and altered mental status
Rigidity/hyperthermia causes muscle damage/nectosis, which elevated blood creatine kinase, myoglobin broken down and pissed out, LDH elevated....
Can progress to rhabdomyolysis which leads to hyperkalemia, hyperphosphatemia, hyperuricemia, AND hypocalcemia.
Stop all antipsychotics
In addition, NMS can be treated with dantrolene (!!) or dopamine agonists such as bromocriptine to bring dopamine levels up.
Atypical Antipsychotics: block 5-HT2, dopamine, α1, and H1 receptors and are associated with less extrapyramidal side effects than traditional antipsychotics
, such as olanzapine, risperidone, and quetiapine, are less likely to cause extra-pyramidal symptoms but are more likely to cause metabolic effects and other miscellaneous side effects.
(sedation, weight gain, constipation, headaches)
True diverticulum (so it contains ALL 3 layers, mucosa, submucosa, muscular layer) in the small bowel and is connected to the ileum!!! .....due to a persistent vitelline aka omphalomesenteric duct.
Can be either:
1) completely persistent vitelline duct (passing meconium via umbilicus, called a vitelline fistula)
2) partial closing (which is Meckel's) . In Meckel's, the patent portion is attached to the ileum!!!
Most common congenital GI anomaly (2% of population) - often found during first 2 years of life
May contain ectopic gastric or pancreatic tissue (!!!!) (gastric is most common, also pancreatic, colonic, jejunal, even endometrial....
intermittent rectal bleeding (can be major) from the ectopic gastric tissue, periublinicul pain, ulcers
Also assoc w/ intussusception/volvulus
Technetium-99m scan diagnoses it!!!!!!!!
A technetium-99m (99mTc) pertechnetate scan, also called Meckel scan, is the investigation of choice to diagnose Meckel's diverticula in children. This scan detects gastric mucosa; since approximately 50% of symptomatic Meckel's diverticula have ectopic gastric or pancreatic cells contained within them, this is displayed as a spot on the scan distant from the stomach itself.
Chlamydia trachomatis is divided into several serotypes.
- A, B, C- chronic infection causes trachoma aka follicular conjunctivitis in Africa. (ABC= Africa, Blindness, Chronic Infection)...... transmitted by hand-eye contact, causing eye inflammation, corneal vascularization, scarring, and blindness.
- D-K causes urogenital infections (PID, ectopics), and neonatal conjunctivitis and pneumonia (can be passed through birth canal)
- L1-L3 causes lymphogranuloma Venereum
Neisseria are diplococcic gram negative, with flattened sides sometimes referred to as kidney bean-shaped.
• Neisseria produce IgA protease, which allows for oropharynx colonization.
• Deficiency in the complement factors C5-C9, also known as the membrane attack complex (MAC), predisposes to Neisseria bacteremia. !!!!!!!!!! !
• Meningococcal meningitis (from N. meningitidis) often result in shock and disseminated intravascular coagulation that can lead to adrenal infarction, a syndrome known as Waterhouse-Friderichsen syndrome. !!!!
• LOS (lipooligosaccharide !!!!!) is a component of the outer membrane of N. meningitidis. This acts as an endotoxin and is responsible for septic shock and hemorrhage, as seen in Waterhouse-Friderichsen syndrome. Plasma levels of LOS highly correlate with the severity of infection !!!!! (ie, high LOS causes a more severe shock, DIC, etc!!!!!!)
N. Meningitis colonizes in the nasopharynx, then goes to the blood, then into the choroid plexus, then the meniges !!!!!!!!!!!!
N. meningitidis causes meningitis and meningococcemia with petechial rash.
N. gonorrheae ferments glucose; N. meningitidis ferments glucose and maltose.
Note: Pilli are requires for infection!!!!!!
The Pilli undergo antigenic variation!!!
Occurs 5-10 weeks later later, it is a disseminated disease with constitutional symptoms including fever, sore throat, malaise, lymphadenopathy. After secondary infection, the virus can become latent.
Presents with symmetric, non-pruritic RASH on palms and soles of feet. This rash can be macular, papular or pustular in appearance.
Can also have a Condyloma lata, which are smooth, flat, lesions that occur in moist, intertriginous regions (perianal area, vulva, scrotum). These lesions hold a high accumulation of spirochetes and are highly infectious
Characterized by gummas, which are PAINLESS soft, non-cancerous growth resulting from the tertiary stage of syphilis. It is a form of granuloma.
Gummas are most commonly found in the liver, but can also be found in brain, heart, skin, bone, testis, and other tissues, leading to a variety of potential problems including neurological disorders or heart valve disease.
- Aortitis, aortic insufficiency, aortic aneurysm with destruction of the vasa vasorum. !!!!!!!!
- Dorsal column demyelination: Neurosyphilis (tabes dorsalis)
-Argyll-Robertson pupils (ARP= Accommodation Reflex Present .. And PRA = Pupillary Reflex Absent)
- broad-based ataxia
Efficacy = maximum effect!!
In spare receptor theory, a maximal physiological effect of a drug is often met with increasing concentration of the drug, however maximal effect is reached before all receptors are bound (i.e. there are spare receptors left over).
In spare receptor theory, a second messenger amplification system could lead to a maximal response despite only a few extracellular sites being activated. For example, G-coupled receptors.
In the presence of spare receptors, noncompetitive antagonists act to "remove" the number of active receptors from the pool of receptors.
• In low dose administration of a noncompetitive antagonist only the spare receptors are bound, allowing agonist to bind to available, or "non-spare," receptors. This causes a right shift in the dose-response curve.
• In high dose administration of a noncompetitive antagonist, both spare and "non-spare" receptors are bound, preventing agonist to bind to any receptors. This results in a downward shift of the dose-response curve.
diazepam, lorazepam, midazolam, chlordiazepoxide
Benzodiazepines modulate GABA by binding to a specific ALLOSTERIC regulatory site (the benzodiazepine receptor) on the GABA-A receptor: this site is distinct from the GABA binding site but binding of the benzodiazpeine to its site increases the affinity of GABA for the receptor.
Note: benzo's, barbs, and alcohol ALL bind to GABA-A.
Binding of GABA to its receptor triggers an opening of a Cl- channel which leads to an increase in Cl- conductance by increasing the frequency of opening, and thus by increasing the efficiency of GABA, to decrease the excitability of neurons. This reduces the communication between neurons and, therefore, has a calming effect on many of the functions of the brain.
NOTE: Since benzo's increase the effectiveness of GABA, they are NOT effective if there is no GABA.
# Intoxication: minor respiratory depression, somnolence (sleepiness), slurred speech, ataxia, some amnesia, confusion.
Falls are common in elderly, ESPECIALLY long acting ones.
Withdrawal: sleep disturbance, depression, rebound anxiety
Long acting benzos, high risk of severe drowsiness and falls
Short acting benzos, high risk of physical dependence.
Either anaphylactic (bee stings, some foods/drugs).....or atopic/allergic (hay fever, rhinitis, asthma, eczema, etc)
Initial antigen exposure stimulates production of IgE antibodies‚ which attach to the surface of mast cells.
• Re-exposure to same antigen → crosslinking of surface bound IgE molecules !!!! → degranulation of basophils and mast cells which release histamineamine*. This initiates the immediate phase of the reaction. which causes itching; bronchospasm‚ wheezing‚ and shortness of breath; and vasodilation and edema formation with low blood pressure‚ weakness‚ and tissue swelling.
• Immediate Phase: Release of histamine, tryptase (!!), kinogenase (!!!), prostaglandins, platelet aggregating factor, and ECF-A. Since no products need to be synthesized by the cell, this process is rapid. !!!!!
While the initial phase is in progress, the cell also begins synthesizing leukotrienes and their derivatives as a part of the late phase of the reaction. The products of the late phase reaction are inflammatory and attract neutrophils and eosinophils.
Eosinophils are recruited to the site of inflammation as a part of the late-phase reaction. Once present, they release several mediators, among them arylsulfatase and histaminase which can act to decrease the severity of inflammation. However, LTC4 and PAF are also released which overall activate mast cells to further release cytokines.
Thus, eosinophils are now believed to amplify and sustain the inflammatory response, thus necessitating treatment with corticosteroids.
The most common causes of cardiac tamponade include dissection of aortic aneurysm, end-stage lung cancer, heart attack, heart surgery, pericarditis caused by bacterial or viral infections, and wounds to the heart.
Patients with hypothyroidism, uremia, or collagen vascular disease (e.g., lupus, rhuematoid arthritis, scleroderma) may have asymptomatic effusions since fluid build-up occurs gradually.
is an unenveloped (naked capsid), single-stranded RNA virus with a cubic (icosahedral) symmetry.
# Hep A spread and complications
It is commonlt a "anicteric" (subclinical, no jaundice!!) infection in young children!!!! (anti-hepatitis A IgG is present)
fecal-oral, uncooked food/seafood, contaminated water. Commonly TRAVELERS. (!!!!!!) (ie, people who travel to shitty/crowded placed).
BOILING WATER Kills hep A !!!!!! (not just heating it, it has to be BOILED)
Most likely hepatitis to produce Jaundice
-most recover, liver damage reversed, no carrier state
- produces fever, malaise, nausea, vomiting, etc.
1. Portal hypertension because of mostly fibrosis obstructing blood flow through portal vein , which causes:
- Ascites (fluid in peritoneal cavity from increased hydrostatic pressue)
- splenomegaly and hypersplenism (consumption of platelets and RBCs from enlarged spleen)
- distended abdomen (
- Portosystemic shunts (esophageal varicies, hemorrhoids, caput medusae)
- liver failure
- hepatorenal syndrome (rapidly developing kidney vasoconstriction/failure due to liver. Often requires liver transplant)
2. Decreased detoxification (mental changes, asterixis, b/c NH4)... but is REVERSABLE.
-Also, excess estrogen and its sides. (palmar erythema, spider nevi, gynecomastia, testicular atrophy)
3. Decreased protein synthesis (hypoambuminemia leading to edema, coagulopathy due to decrease clotting factors, epoxide reductase)
Also Anorexia, Weight loss, Weakness, Hepatocellular carcinoma
Mechanism: IRREVERSIBLY Inhibits vitamin K-dependent γ-carboxylation of factors X, IX, VII, II ("1972"), protein C, and protein S
"EX president, War, 10,9,7,2)
→ effects last 7-10 days after stopping therapy.
Given for CHRONIC anticoagulation (atrial fibrillation, DVT/PE, cardiac valve replacements), Follow PT or INR (normalized version of PT)
e.g., nitroprusside, nitroglycerin, isosorbide dinitrate
Mechanism: forms nitric oxide (NO), a free radical that activates guanylate cyclase → increased cGMP in smooth muscle → vasodilatation .
Nnitrates have greater effect on large veins and therefore cause decreased preload, aka left ventricular filling volume !!!!!! They do this by reducing venous return (blood is retained in the venous system).... more so than reducing afterload. !!
This reduced preload causes decreased myocardial oxygen consumption, increases coronary blood flow, improving ischemia.
A decrease in preload decreases stroke volume (Frank Starling mechanism), as well as CO, end systolic left ventricle volume, and afterload.
Thus, there is a compensatory INCREASE HEART RATE!!!! .
NO is normally produced by the endothelial cells of the blood vessel, but the action of NO is on the smooth muscle cells.
preglomerular resistance INCREASES with NSAID's because prostaglandins are vasodilators. In patients with states of volume depletion (heart failure, cirrhosis), there is an INCREASED secretion of vasoconstrictors, angiotensin II, norepinephrine.
Thus, in these cases, prostaglandins are essential to maintain renal blood flow and counteract vasoconstrictive effects at the afferent arteriole.
therefore, in volume depleted patients, NSAID's cause renal flow and thus, GFR to DECREASE, causing ischemia and acute renal failure.
Histopathologically, small cell lung carcinoma has a distinct morphology consisting of poorly differentiated, small, round, oval or spindle shaped hyperchromatic, hypermitotic cells with a granular salt-and-pepper nuclear chromatin pattern.
ALL small cell lung carcinomas are high grade, highly malignant and widely metastatic. Small cell lung carcinomas are the most aggressive* of all lung carcinomas
Extensive necrosis is common in small cell lung carcinoma.
Small cell lung cancer, like squamous cell lung cancer, more commonly arises centrally near the hilum or major bronchi !!!
Mnemonic: when it starts with "S" it is associated with Smoking, "sen"tral, and maybe paraneoplastic syndrome.
The chorion is set at day 3 !!
1) If cleavage occurs at day 1-3 as a Morula, BEFORE the chorion formed, each twin will have:
- their own chorion (dichorionic) and therefore each will have its
- own placenta and amniotic sac (diamniotic).
2) If cleavage occurs after day 3, the cells that have been set to become the chorion have already been formed, so there is only ONE shared chorion for both twins (monochorionic), and thus ONE placenta that is shared.
A) If cleavage is day 4-8, the twins are monochorionic diamniotic ( one chorion, one placenta, each has its own amniotic sac).
B) If cleavage is day 8-13, the twins are monochorionic monoamniotic (one chorion, placenta, amniotic sac that they share),
C) If cleavage is day 13-15, the twins are "conjoined" with a single chorion, placenta and amniotic sac.
1. Antihistaminic (sedation and weight gain)
2. Antiadrenergic alpha 1 (orthostatic HYPOtension, tachycardia, and arrhythmias)
3. Anticholinergic muscarinic (dry mouth, dilated pupils, tachycardia, hyperthermia, confusion, constipation/intestinal ileus, and urinary retention !!!)
4. can cause Anti-cholinergic sides .... "red as a beet (flushing), dry as a bone (anhidrosis), hot as a hair, blind as a bat (blurred vision), mad as a hatter (hallucinations/delirium), full as a flask (urinary retention)"
Characterized by loss of control binge eating (ie, entire pizzas) FOLLOWED by feeling depressed about it, and then either:
- Purging, which includes (vomiting or abuse of laxatives, diuretics, or enemas.)
- Non-purging (excessive exercising, dieting, fasting)
• Body weight is USUALLY normal or slightly overweight. (not always though)
• Associated with esophageal tears (Mallory-Weiss syndrome) and rupture (Boerhaave syndrome), dental caries/erosions, swelling of parotid glands (facial swelling, electrolyte disturbances, menstrual irregularities, alkalosis, and dorsal hand calluses from inducing vomiting (Russell's sign), calluses on the knuckles.
Hepatic encephalopathy (also known as portosystemic encephalopathy) is the occurrence of:
- confusion/altered level of consciousness
- ataxia & hyperactive deep tendon reflexes
- signs of chronic liver disease (jaundice, edema, ascites, palmar erythema, telangiectasias, caput medusa)
and coma as a result of liver failure!! (hepatitis, HCC, etc)
Encephalopathy occurs due to buildup of ammonia, which is normally converted to urea in the liver!!
Ammonia can cross blood brain barrier, and causes:
- increased inhibitory neurotransmission (GABA)
- Impaired excitatory neurotransmitter release (glutamate)
Hypeammonia toxicity depletes glutaMATE and alpha-ketoglutarate in the brain!!!!.
There is accumulation of glutaMINE, which causes astrocyte swelling
5α-reductase deficiency is a AR inherited disorder resulting in an inability to convert testosterone to dihydrotestosterone (DHT). Limited to genetic males (46 XY).
Testosterone is responsible for development of male genitalia during embryogenesis, spermatogenesis,.
DHT mediates development of external genitalia (penis/scrotum), growth of prostate, facial hair and hairline recession.
At birth, external genitalia are predominantly female OR very underdeveloped for males..... and patients are often raised as females. Then, virilization (enlargement of the phallus, increases in body hair and muscularity, voice deepening, no breast development) occurs during puberty due to increasing levels of testosterone.
Patient has male internal organs, and person fails to menstruate.
Cells undergo apoptosis (ie, from DNA damage), and release nuclear debris. self reactive B-lymphocyte may be exposed, and it produces anti-nuclear antigens.
Antigen-antibody complexes are deposited in multiple tissues, and this activates complement, which damages those tissues. (Type 3 HSR)
S/Sx: joint/muscle/chest pain, headaches, fever, oral ulcers, rashes, damages serosa.
Destruction of cells in the blood, so antibodies against: (this is Type 2 HSR!!!) It produces a pancytopenia!!!!
- RBCs lead to anemia,
- against platelets thryombocytopenia
- against WBCs leads to leukopenia.
Common death causes are renal failure and infection (antibodies destroy WBCs).
30% of patients get antiphospholipid syndrome (anti cardiolipin, lupus anticoagulant. Latter makes patient HYPER coaguable, produce thrombosis in both arteries (stroke) and veins (DVT, Budd Chiari in hepatic vein),
Excessive cortisol, so muscle wasting (weakness, thin extremities)
- Moon facies, buffalo hump, truncal obesity (excess glucose, so excess insulin, and fat stores in face, back, trunk)
- abdominal striae (cortisol impairs collagen synthesis, so weak collagen leads to easy blood vessel rupture)
- HTN (cortisol upregulated Alpha-1 receptors on arterioles to upregulate vascular tone
- Osteoporosis, immune suppression
- most common form of necrosis !!!!
often caused by interruption of blood supply → tissue ischemiaa* → intracellular accumulation of lactic acid → denaturation of structural proteins FIRST, and THEN denaturation of intracellular enzymes
Necrotic tissue that remains firm, cellular proteins coagulate so that cell shape and structure are preserved.
"Tissue dies, but general structure of tissue remains, cells and their architcture are present, but NUCLEI DISAPPEAR"!!!!!!!!
Seen with ischemia in ANY organ except brain. Occurs most commonly in organs supplied by end arteries with limited collateral circulation such as heart, kidney, and spleen
Area of infarcted tissue often kinda WEDGE SHAPED and PALE. Usually when a vessel goes into tissue it branches in two... if you stop blood, everything around it dies (wedge shaped). Wedge POINTS to area of occlusion.
Can get "Red infarction" if blood re-enters tissue, and tissue is loosely organizes (ie, pulmonary or testicular infarcts).
Energy dependent, genetically programmed cell death, usually in single or small groups of cells.
Always by caspases!!! Caspases are activated by:
1. Initiation stimuli through either :
a) Intrinsic mitochondria mediated pathway ((Bcl-2, apaf-1, cytc etc....) This is induced by things like UV radiation, heat, hypoxia, toxins
b) extrinsic, receptor-ligand induced pathway . (controlled by TNF or FAS-L!!!)
2. Execution/Control stage, either the (Bcl-2, apaf-1, cytc etc)... or
3. Both pathways converse activating caspases