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41 Cards in this Set

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Cardiogenic (and obstructive) shock
Failure of cardiac pump due to intrinsic myocardial injury, pressure, or outflow obstruction

(MI, ventricular rupture, arrhythmia, cardiac tamponade, pulmonary embolus)
Hypovolemic Shock
Fluid loss (hemorrhage, vomiting, diarrhea, burns); compensatory mechanisms include sympathetic discharge (tachycardia, increased contractility, vasoconstriction); activation of renin-angiotensin pathway for volume conservation. Arterial BP is maintained up until a 20% loss in blood volume.
Anaphylaxis
Hypersensitivity reactoin; systemic vasodilation due to IgE mediated hypersensitivity

Histamine released; massive vasodilation
Septic Shock
Microbial infection; causes peripheral vasodilation and pooling of blood, endothelial activation/injury, leukocyte induced damage, DIC, activation of cytokine cascades
Stages of Shock
Effects of Shock
Effects of Shock on the Heart
Petechial hemorrhages seen on the epicardium and endocardium.
On microscopic examination there may be foci of necrosis involving the myocardium. These can range from loss of single fibers to large regions of necrosis. Contraction bands can be seen.
Acute Tubular Necrosis in the Kidneys
Effects of shock on lungs; Injury to the alveolar walls can result in shock lung which can cause acute respiratory distress syndrome (ARDS).
Acute lung injury results in impaired gas exchange and other effects. There is increase in the work of breathing, respiratory muscle fatigue causing ventilatory failure. Mechanical ventilation may be required.
Shock GI; Focal ischemic necrosis of colonic mucosa; can lead to diffuse GI hemorrhage due to gastric mucosal erosions and upserficial ischemic necrosis of the intestines; compromise in the barrier function of the intestine can result in septicemia
shock liver; necrosis of the central area of a liver lobule due to severe circulatory shock

most common finding in shock related to the liver is mild increase in aminotransferaes and LDH; w severe hypoperfusion shock liver can result in massive aminotransferase levels and extensive hepatocellular damage; there may be decreases in albumin and clotting factors; shock can result in centrilobular congestion and necrosis
Effects of shock on pancreas
The pancreas is supplied by the splanchnic vascular bed which is susceptible to impaired circulation.
Ischemic damage of the pancreas can result in the release of catalytic enzymes which can further promote shock.
Effects of shock on brain
In severe cases of shock, especially in patients with cerebral atherosclerosis, necrosis and hemorrhage may occur with watershed infarcts.
Watershed (border zone) infarcts are those that occur between the ends of arterial territories. In the cerebral hemispheres the region between the anterior and middle cerebral arteries is at greatest risk.
In cases of severe shock adrenal glands can develop hemorrhage involving the inner cortex.
Waterhouse-Friderichsen syndrome is massive hemorrhage and necrosis involving the entire gland and is classically seen with meningococcal septicemia.
Hypertension Cutoff
>140/90
Prehypertension Cutoff
>120/80
Essential (primary) hypertension vs secondary hypertension

Which is more frequent
Primary HTN (95%)

Secondary causes include endocrine, renal, cardiovascular
Essential (primary) hypertension
Elevations of bp wo any identifiable cause

multifactorial disorder, including eentic and environmental components
Accelerated/Maligant Hypertension
Severe hypertension (>200/120), renal failure, retinal hemorrhages, exudates, papilledema

Can arise in normotensive individuals but usually is spuerimpoesd on pre-existing benign htn
Hyaline Arteriosclerosis; due to chronic htn results in variable increases in arterial wall thicknes
Hyperplastic ARteriosclerosis; onion skin lesion; seen in SEVERE HYPERTENSION (>200); reduplicated basement membranes
necrotizing arteriolitis/fibrinoid necrosis; Vascular damage causes necrosis of the vessel wall and increased permeability of the vessel to fibrinogen and other proteins; narrowed lumen
Progression/complication of atherosclerosis
artherosclerosis; A section of a coronary artery showing a fibrous cap (F), a central necrotic (mostly lipid) core (C) in which the lumen (L) has been compromised.
atherosclerosis; This is an acute coronary thrombosis atop a fibrous cap. This event resulted in a fatal myocardial infarction.
Aortic Dissection; hypertension is the major risk factor
Two most important effects of hypertension on the heart
Increased afterload; accelerated atherosclerosis of the coronary arteries
Chronic hypertension;

C = normal myocardium, D = increase in cell size and nuclear size in the hypertrophied myocytes boxcar)
Normal heart on right

Left ventricular hypertrophy on left
Lacunar infarct; due to deep penetrating arteries involved in small vessel strokes
Lacunar infarct; due to deep penetrating arteries involved in small vessel strokes
Section from a lacunar infarct; notice the cystic space
Hypertensive Hemorrhage in basal ganglia; hypertension weakens the walls of the small penetrating vessels
Nephrosclerosis
htn induced kidney disease; leading cause of renal failure; blood vessel walls thickened w hyaline material (hyaline arteriosclerosis)
somoth muscle hypertrophy/necrosis (fibrinoid necrosis)
Malignant hypertension
A: fibrinoid necosis of the afferent arteriole
B: hyperplastic arteriolitis (onion skinning)
Flea bitten kidney; effect of malignant htn on kidney; notice small petechiae
Normal retina
Arteriovenous nicking; due to thickened retinal arterioles; this is bc retinal arteries/veins where they cross
Cotton wool spots?
These represent small retinal infarcts and swelling of the nerve fiber layer of the retina. They can be seen in disorders that affect the retinal microvasculature including hypertension.
Exudates?
Hard exudates are deeper in the retina than cotton wool spots and are produced by leaky damaged vessel walls. Leakage of serum and lipid aggregates cause accumulations of lipoproteins hence the waxy and glistening look of these lesions.
Flame hemorrhage?
When hemorrhages occur in the superficial layer (nerve fiber layer) of the retina it is oriented with the nerve fibers and is linear (flame –shaped). These types are most common in hypertension