Week 3 Borch Flashcards
Why are heart and lungs in series? Why are other organs in parallel?
Series – when input needs to match output – we want blood entering heart = blood leaving lungs, otherwise we have shunting or a mega fluid shift
Parallel – so that blood flow to one organ doesn’t have a huge effect to flow to other organs
Give overview of blood flow from Right atrium to vena cava. Give the general function of each part. Give relative pressures of each component of system.
RA – LA – PA (low pressure) – lungs – PV – LA –LV – Aorta/systemic arteries (high pressure) (conducting/distributing) – arterioles (resistance vessels) – capillaries (exchange) – venules – veins (capacitance) – S/IVC
What is portal circulation? Give 2 examples.
2 capillary beds in series. Liver and Kidney (ie filter organs)
Name 3 layers and components of generic blood vessel wall.
Tunica Intima – endothelium, loose CT, internal elastic lamina
Tunica media – smooth muscle, collagen, elastic tissue
Tunica adventitia – collagen, external elastic lamina
Describe the forces that help prevent edema. Describe the system that helps resolve edema.
Edema prevented by balance between hydrostatic pressure from the fluid column entering the capillaries (causing nutrients to be pushed out into tissues), and oncotic pressure from the luminal contents leaving the capillaries (ie osmotic pressure of proteins that can’t permeate the membrane, causing fluid to return to the vasculature.
If it occurs, lymphatic drainage helps re-circulate it
Give 5 mechanisms for edema formation.
Increased hydrostatic pressure (ie heart failure and pulm edema)
Reduced oncotic pressure (conditions that cause low protein – nephrotic syndrome or cirrhosis)
Sodium retention (renal/heart failure)
Increased vasopermability (ie vascular collapse - anaphylaxis, sepsis)
Lymphedema – lymphatic obstruction
Effusion – fluid collection in a body space, not in an organ parenchyma
Differentiate Effusion and Edema by definition and on medical imaging.
Effusion is specifically fluid collection in a body space.
Effusions will “layer out” with different body positions on imaging, due to effects of gravity.
Thorax – Pl effusion, Peritoneum – Ascites, pericardium – pericardial eff, General - Anasarca
Hyperemia vs congestion?
Hyperemia – increase blood due to arteriolar dilation (ie increase inflow)
Congestion – increase blood due to venous obstruction (ie decrease outflow)
Differentiate Left sided vs Right sided heart failure by symptoms.
Both will cause CONGESTION (construction on the interstate, blood gets backed up)
Left sided – traffic jam backs up into lungs, causes pulm edema and patient has SOB
Right sided – traffic jam backs up into organ systems, especially liver, and patient may have multiple sx, including ascites.
Thrombosis vs Clot?
Thrombus is a clot that forms inside the vasculature
Name the 3 nefarious things that work in synergy to cause thrombosis.
Virchow’s Triad: vascular damage, blood stasis/abnormal flow, hypercoagulable state
Differentiate which organs will be effected by arterial and venous thromboemboli.
Arterial – break off on way from heart – get stuck in smaller arterioles – cause gangrene and small organ infarcts
Venous – break off on way back to heart, get pumped thru heart and stuck in pulmonary tree – cause Pulmonary emboli, acute infarct/loss of gas exchange ability in effected lung parenchyma
Differentiate between red and white infarcts. Name two organs that characteristically have red infarcts.
Red – hemorrhagic
White/pale – ischemic
Lung and Bowel are usually hemorrhagic (remember, Liver is weird)
Differentiate among petechiae, purpura, and ecchymoses
Petechiae – 1-2mm hemorrhage in skin or mucous membrane
Purpura - >3mm
Ecchymoses – 1-2 cm (the classical “bruise”)
From LDL to complicated atheroma, describe the formation of atherosclerotic plaques.
Excess LDL gets stuck in intima, behind endothelium, oxidizes and causes local damage. This makes endothelium express inflammatory markers which flag monocytes to roll in and phagocytose the offending LDL particles. The monocytes (now macrophages) have “bit off more than they can chew,” and get stuck, becoming “foamy macrophages” which cause even more damage to surrounding area. Smooth muscle cells migrate in from media, proliferate and lay down more ECM, causing a mass effect to displace endothelium into lumen (the uncomplicated atheroma). Over time, this may continue, and the endothelium over the atheroma may rupture, causing further inflammation and clotting factor activation, thrombus, etc. – the complicated atheroma
What does necrosis look like on H&E? Why?
Red/Pink – no nuclei are left to be stained blue by the Hematoxylin. Mummified.
Atrophy
smaller cells, less cells, less function
Hypertrophy
Larger cells
Hyperplasia
more cells
Metaplasia
change in cell type
What happens when a cell runs out of ATP?
Na/K Pump stops working – influx of Na, water follows, POP goes the cell!
Increase in glycolysis – lowers pH, enzymes stop working as well
Influx of Ca – binds/interacts with what it’s not supposed to, causing widespread damage by activation of autolytic enzymes
Name 5 categories of Necrosis. Try to give examples of each.
Coagulative – firm, structurally intact (infarct)
Liquefactive – juicy, no structural integrity (abscess or brain infarct)
Caseous – cheesy (almost always TB)
Fat – fatty, within fat (pancreatitis, saponification, calcification), varying size of fat globules
Fibrinoid – assoc with fibrin deposition around vessels (microscopic only)
Name 4 cell types that eat things (phagocytosis).
Neutrophils, Macrophages, Dendritic Cells, Mast cells
Name 4 cell types that present antigens.
Dendritic cells, Macrophages, Mast cells, and B cells
Name the major function of Mast cells, basophils, and Natural Killer cells. How are Killer T’s different?
Mast cells + basophils – histamine release, dealing with parasites, mediating allergic reactions
Natural Killer cells – kill anything that doesn’t express MHC1 (ie. Prevent cells circumventing the MHC1 “kill me now” pathway). Killer T’s will kill a cell showing something suspicious on its MHC1.
Name the cell type most associated with acute inflammation.
Neutrophils
Name the 4 clinical signs of acute inflammation and their etiologies
Rubor (redness, from vasodilation), Dolor (pain – from inflammatory cytokines), Calor (heat, from vasodilation), Tumor (swelling – from increased hydrostatic pressure causing fluid transudate)
