Unit 4 - Wk 5 Pathology

Front 1

Cardiogenic (and obstructive) shock

Back 1

Failure of cardiac pump due to intrinsic myocardial injury, pressure, or outflow obstruction

(MI, ventricular rupture, arrhythmia, cardiac tamponade, pulmonary embolus)

Front 2

Hypovolemic Shock

Back 2

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.

Front 3

Anaphylaxis

Back 3

Hypersensitivity reactoin; systemic vasodilation due to IgE mediated hypersensitivity

Histamine released; massive vasodilation

Front 4

Septic Shock

Back 4

Microbial infection; causes peripheral vasodilation and pooling of blood, endothelial activation/injury, leukocyte induced damage, DIC, activation of cytokine cascades

Front 5

Stages of Shock

Back 5

Front 6

Effects of Shock

Back 6

Front 7

Effects of Shock on the Heart

Back 7

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.

Front 8

Back 8

Acute Tubular Necrosis in the Kidneys

Front 9

Back 9

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.

Front 10

Back 10

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

Front 11

Back 11

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

Front 12

Effects of shock on pancreas

Back 12

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.

Front 13

Effects of shock on brain

Back 13

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.

Front 14

Back 14

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.

Front 15

Hypertension Cutoff

Back 15

>140/90

Front 16

Prehypertension Cutoff

Back 16

>120/80

Front 17

Essential (primary) hypertension vs secondary hypertension

Which is more frequent

Back 17

Primary HTN (95%)

Secondary causes include endocrine, renal, cardiovascular

Front 18

Essential (primary) hypertension

Back 18

Elevations of bp wo any identifiable cause

multifactorial disorder, including eentic and environmental components

Front 19

Accelerated/Maligant Hypertension

Back 19

Severe hypertension (>200/120), renal failure, retinal hemorrhages, exudates, papilledema

Can arise in normotensive individuals but usually is spuerimpoesd on pre-existing benign htn

Front 20

Back 20

Hyaline Arteriosclerosis; due to chronic htn results in variable increases in arterial wall thicknes

Front 21

Back 21

Hyperplastic ARteriosclerosis; onion skin lesion; seen in SEVERE HYPERTENSION (>200); reduplicated basement membranes

Front 22

Back 22

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

Front 23

Progression/complication of atherosclerosis

Back 23

Front 24

Back 24

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.

Front 25

Back 25

atherosclerosis; This is an acute coronary thrombosis atop a fibrous cap. This event resulted in a fatal myocardial infarction.

Front 26

Back 26

Aortic Dissection; hypertension is the major risk factor

Front 27

Two most important effects of hypertension on the heart

Back 27

Increased afterload; accelerated atherosclerosis of the coronary arteries

Front 28

Back 28

Chronic hypertension;

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

Front 29

Back 29

Normal heart on right

Left ventricular hypertrophy on left

Back 30

Lacunar infarct; due to deep penetrating arteries involved in small vessel strokes

Front 31

Back 31

Lacunar infarct; due to deep penetrating arteries involved in small vessel strokes

Front 32

Back 32

Section from a lacunar infarct; notice the cystic space

Front 33

Back 33

Hypertensive Hemorrhage in basal ganglia; hypertension weakens the walls of the small penetrating vessels

Front 34

Nephrosclerosis

Back 34

htn induced kidney disease; leading cause of renal failure; blood vessel walls thickened w hyaline material (hyaline arteriosclerosis)
somoth muscle hypertrophy/necrosis (fibrinoid necrosis)

Front 35

Back 35

Malignant hypertension
A: fibrinoid necosis of the afferent arteriole
B: hyperplastic arteriolitis (onion skinning)

Front 36

Back 36

Flea bitten kidney; effect of malignant htn on kidney; notice small petechiae

Front 37

Back 37

Normal retina

Front 38

Back 38

Arteriovenous nicking; due to thickened retinal arterioles; this is bc retinal arteries/veins where they cross

Front 39

Cotton wool spots?

Back 39

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.

Front 40

Exudates?

Back 40

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.

Front 41

Flame hemorrhage?

Back 41

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