Physio Flashcards

Question

What are differentials for hypernatremia in a patient that is assessed to be hypovolemic?

Answer 1

Extrarenal — GI: vomiting, diarrhea, small intestinal obstruction, Third space loss: pancreatitis peritonitis, Cutaneous: burns Renal causes: appropriate: osmotic diuresis (mannitol, hyperglycemia), chemical diuresis (furosemide, ethacrynic acid) Inappropriate: chronic renal failure,nonoliguric acute renal failure, post obstructive diuresis

Answer 2

D5W Formula for correction over 48 hours with goal of not changing serum sodium concentration faster that 0.5 mEq/kg/hr Current weight x (current Na/ normal Na - 1) Can also consider treatment with loop diuretic to promote sodium excretion and help normalize ECF volume

Answer 3

Afghan hounds

Answer 4

V2 receptor mutations (Huskies) | AQP2 channel mutation

Answer 5

Drugs - steroids, lithium, E. Coli endotoxin, diuretics Electrolyte disturbances - hypokalemia, hypercalcemia Altered medullary hypertonicity - hypoadrenocorticism Multifactorial/ unknown mechanism - hepatic insufficiency, hyperthyroidism, hyperadrenocorticism Post obstructive diuresis Acromegaly Medullary interstitial amyloidosis Poly cystic kidney disease Chronic pyelonephritis Chronic interstitial nephritis

Answer 6

Correct underlying cause If primary: dietary sodium restriction Thiazide diuretics - used to induce mild dehydration ,enhanced proximal renal tubular resorption of sodium, decreased delivery of tubular fluid to distal nephron and reduced urine output

Answer 7

Hyperlipidemia, hyperproteinemia (I.e. pseudo hyponatremia)

Answer 8

Hypervolemia: severe liver disease, CHF, nephrotic syndrome advanced renal failure Normovolemia: psychogenic polydipsia, SIADH, antidiuretic drugs, myxedema coma, hypotonic fluids Hypovolemia — nonrenal - GI loss (vomiting, diarrhea), third space loss (pancreatitis, peritonitis, pleural effusion, uroabdomen) REnal route - hypoadrenocorticism, diuretic administration

Answer 9

Hyperglycemia, mannitol infusion — increased presence of sodium free solute draws fluid into the intramuscular space Each 100 mg/dL glucose reduces Na by 2.4 mEq/L

Answer 10

RAAS overactivation due to severe liver disease, CHF, nephrotic syndrome, advanced renal disease, etc ADH release Primary intrarenal sodium retention. - found occurring due to nephrotic syndrome only (based on normal renin and aldosterone levels in certain patients with nephrotic syndrome)

Answer 11

Osmotic demyelination - when hyponatremia is corrected faster than the brain can re-establish idiogenic osmoles

Answer 12

Inappropriately high urine osmolality in the presence of plasma hypoosmolality Normal adrenal, renal ,and thyroid function Presence of natriuresis despite hyponatremia and plasma hypoosmolality as a result of mild volume expansion No evidence of hypovolemia No evidence of ascites or edema Correction of hyponatremia with fluid restriction

Answer 13

Occurs in people with intracranial injury, differentiated from SIADH as water and sodium replacement are needed in cerebral salt wasting syndrome while water restriction is needed for SIADH Caused by atrial and brain natriuretic factors Treatment = fluid therapy and fludricortisone (Facilitates sodium retention)

Answer 14

1. Increased thrombin production 2. Suppression of physiologic anticoagulant pathways 3. Impaired fibrinolysis 4. Activation of inflammatory pathways

Answer 15

Tissue factor (aka TF, coagulation factor III, tissue thromboplastin It is expressed on monocytes and endothelial cells within circulation during inflammation and on malignant cells in cancer patients It is a transmembrane protein that is not typically exposed to general circulation, but increased exposure to circulation leads to DIC It is released into circulation in response to pro-inflammatory cytokines (they induce monocytes/ macrophages to express tissue factor)

Answer 16

IL 1 - increases platelet reactivity, increases TF expression in vitro, most procoagulant changes occur before detectable in Vito Il6 - principle mediator of coagulation activation TNFa - influences coagulation directly through its effects on IL6. Can also perpetuate inflammation by induction of NFkB —> TNFa Endotoxin

Answer 17

Systemic infection, trauma, burns, heatstroke, cancer

Answer 18

Tissue factor: factor VII a complex (in the extrinsic pathway)

Answer 19

This activates factor IX (intrinsic) and factor X (extrinsic) Activated factor X generates thrombin Thrombin activates factor XI, VII, and V, thus amplifying its own production

Answer 20

Converts fibrinogen to fibrin, which forms strands to support clots

Answer 21

They can alter their morphology and express negatively charged substances on their surface, which enhance prothrombinase and tease They can increase their number of copies of active fibrinogen receptor Secrete granules with procoagulant elements such as calcium, factor Va, serotonin, fibrinogen, P selection and ADP

Answer 22

Antithrombin - potent inhibitor of factor IXa, most effective when bound to heparin like GAGs or exogenous heparins (enhances inhibition by 1000 fold), Binds to inhibit thrombin, and factors IXa, Xa, XIa and TF: VIIa Activated protein C: inhibits factors Va and VIIIa. Effects are enhanced 20 fold when in the presence of protein S. IT prevents thrombin from acting on fibrinogen and platelets. Also produces thrombin activatable fibrinolysis factor (TAFI) Tissue factor pathway inhibitor - inhibits TF:VIIa complexes and factor Xa - this is a potent inhibitor of thrombin generation

Answer 23

It is a network of glycosaminoglycans (GAGs), proteoglycans, and glycoproteins —proteoglycans are 50-90% heparin sulfate, which facilitates antithrombin binding and enhances inhibition of thrombin Other procoagulant also bind to the glycocalyx The glycocalyx also serves as a mechanoreceptor, sensing altered blood flow and releasing nitric oxide during times of increased shear stress to maintain appropriate organ perfusion

Answer 24

Activation of fibrinolysis occurs concurrently with thrombin generation - there is an initial rapid increased in fibrinolytic activity during sepsis/SIRS secondary to release of tissue plasminogen activators from endothelial cells. TPA —> plasminogen —> plasmin —> cleavage of fibrin clot. Increase in plasmin activated complement and kin in systemic which can lead to shock, hypotension, and increased vascular permeability. This results in increased fibrin degradation products (FDPs) from fibrinogen or cross linked fibrin strands). D diners come from cross linked fibrin, FDPs coat platelets to prevent hemostasis and interfere with fibrin polymerization. During DIC, fibrin deposition surpasses fibrinolysis

Answer 25

Inflammatory pathways upregulate TF expression and downregulate inhibitors Activated coagulation proteins stimulate release of inflammatory cytokines Endothelial cells can be activated by inflammatory cytokines (TNFa, bradykinin, thrombin, histamine, and VEGF) —> activated endothelial cells release ultralarge VWF, which increases platelet tethering and activation at site of activated endothelial cells. There is also a decrease in ADAMTS13 (which usually cleaves ULVWF into smaller particles and makes it less potent) Platelet activating factor is also released from inflammatory cells Protein C system is depressed during DIC, so anti inflammatory effects of protein C system are lost

Answer 26

PT/PTT prolongation (PTT is more sensitive indicator due to greater consumption of these factors in DIC) Fibrinogen can be increased or decreased in DIC Degree of thrombocytopenia - continued platelet decrease even within RI is suggestive of thrombin generation D dimer elevation - (this results from plasmin degradation of cross linked fibrin and is specific for fibrinolysis not DIC (can also see increased D diners in thromboembolic disease, trauma, surgery, hemorrhage and neoplasia) The Best combination of tests to obtain the most accurate diagnosis of DIC=. Platelets, aPTT, FDP, D dimer — sensitivity of 73%, specificity of 97%

Answer 27

Elevated FDPs do not distinguish between degradation product of fibrinogen or cross linked fibrin Elevation shows active fibrinolysis, which can occur in trauma, recent surgery, or venous thromboembolism FDPs are metabolized in the liver and excreted in kidneys - dysfunction in either organ can increased FDP

Answer 28

Not generally, it can remain normal even with high consumption Sensitivity of fibrinogen for confirming DIC in people is 28-43%

Answer 29

Decrease - it becomes consumed due to factor activation

Answer 30

Yes, it was positively associated with the severity of DIC

Answer 31

Hypovolemic Cardiogenic Distributive

Answer 32

Hypovolemic - decreased effective circulating volume Distributive - inappropriate vasomotor tone aka vasodilatory shock/ decreased blood flow to vital organs Cardiogenic shock - decreased forward flow, heart can’t pump enough to periphery Obstructive shock - decreased forward flow or decreased venous return Metabolic - abnormal cellular respiration - e,g. Severe metabolic acidosis Hypoxemic shock - decreased arterial oxygen content

Answer 33

``` Peripheral vasoconstriction Increased HR Increased RR RAAS activation ADH release ```

Answer 34

Compensatory - cardiac output is increased due to catecholamine release. This is characterized by a normal BP and mild clinical signs (mild tachycardia, injected mm, rapid CRT) Early decompensatory - blood is preserved for heart and brain perfusion and lactic acidosis and tissue hypoxia occur. This is characterized by hypotension and moderate severe clinical signs (tachycardia, pale mucous membranes, prolonged CRT, depressed mentation and hypothermia) Late decompensatory shock - auto regulatory escape occurs and the Braine and heart can no longer maintain sympathetic mediated vasoconstriction resulting in global vasodilation and circulatory collapse. This is characterized by severe hypotension and severe life threatening clinical signs (bradycardia, absent CRT, weak or absent pulses, hypothermia, obtundation and oliguria)

Answer 35

PH can be characterized by changes in bicarbonate and PCO2 (predictable changes in HCO3 occur with loss or gain of H+) PH = 6.1 +log (HCO3/(0.03 x PCO2))

Answer 36

Amount of base above or below the normal buffer base This is calculated by taking into account the expected change in HCO3 secondary to acute changes in PCO2 Interpretation: HCO3 should rise 1-2 mEq for every acute 10 mmHg increased in pCO2 HCO3 should decrease 1-2 mEq/L for every acute 10 mmHg decrease in PCO2

Answer 37

It exacerbates hypercapnea by donating substrate for carbonic acid equation

Answer 38

Administered in severe academia cases - pH <7.15, bicarb < 12 Dose - 0.3 x body weight x base deficit — half of the dose should be given over 6 hours with reevaluation

Answer 39

Hyperosmolarity Hypernatremia Hypokalemia (alkalosis encourages intracellular shift of potassium) Ionized hypocalcemia (calcium complexes with bicarb) Paradoxical CNS acidosis - due to diffusion of CO2 from bicarb administration across the BBB

Answer 40

``` Low FiO2 Hypoventilation Diffusion impairment VQ mismatch Pulmonary shunting ```

Answer 41

PaO2 - measurement of partial pressure of oxygen - provides an estimation of dissolved O2 in the blood SPO2 - measurement of differences in absorption of two wavelengths of light (red and infrared) by oxygenated and deoxygenated hemoglobin - provides an estimation of hemoglobin saturation.

Answer 42

Carboxyhemoglobinemia and methemoglobinemia

Answer 43

It maintains vascular permeability Shield the walls of the blood vessel from direct blood flow exposure Mediates shear stress dependent nitric oxide production Promotes retention of vascular protection enzymes (superoxide dismutase) Perseveres intravascular coagulation inhibition factors (antithrombin, protein C and tissue factor inhibitor) Modulate the inflammatory response (by preventing leukocyte adhesion and binding of chemo lines, cytokines, and growth factors)

Answer 44

Finite interstitial volume Albumin washout Augmented lymphatic flow

Answer 45

``` Stable clotting factors: II, VI, IX, X Labile clotting factors: V and VIII VWF Fibrinogen Albumin - not useful in treating hypoalbuminemia except in small patients due to potential for hypervolemia. ``` It is stable for 1 year It is indicated in patients with poor oncotic pressure or patients with coagulopathy

Answer 46

Stable clotting factors II, VII, IX, X Fibrinogen Albumin