hemodynamic disorders/thromboembolic ds/shock

Question 1

starling forces

Answer 1

Question 2

pathophysiologic categories of edema

Answer 2

-Increased hydrostatic pressure
-Impaired venous return (e.g., ascites (cirrhosis), congestive heart failure)
-Arteriolar dilation (e.g., heat)

-Reduced plasma osmotic pressure
-Reduced albumin synthesis: severe liver diseases (cirrhosis), protein malnutrition
-Albumin loss: nephrotic syndrome

-Lymphatic obstruction: Trauma, fibrosis, invasive tumors, post-surgery, post-radiation and infectious agents

-Sodium retention – Increased salt retention—with retention of associated water—causes both increased hydrostatic pressure (due to intravascular fluid volume expansion) and diminished vascular colloid osmotic pressure (due to dilution
-e.g., excessive salt intake with renal insufficiency, increased tubular reabsorption of sodium, renal hypoperfusion, increased renin-angiotensin-aldosterone secretion

-Inflammation

Question 3

congestive HF

Answer 3

-INCREASED VENOUS PRESSURE DUE TO HEART FAILURE
-Decreased renal perfusion -> RAAS
-increase hydrostatic/capillary pressure

Question 4

hepatic ascites

Answer 4

-PORTAL HTN
-HYPOALBUMINEMIA
-decrease colloid osmotic pressure
-anasarca

Question 5

renal edema

Answer 5

-SODIUM RETENTION
-PROTEIN LOSING GLOMERULOPATHIES (NEPHROTIC SYNDROME)
-sodium retention -> sodium/water retention
-nephrotic syndrome -> decrease colloid osmotic pressure

Question 6

EDEMA

Answer 6

-Subcutaneous edema: gravity

-pitting edema

-renal dysfunction - loose connective tissue (e.g., eyelids) -> periorbital edema

-pulmonary edema- 2 – 3 X normal weight -> frothy, blood-tinged fluid— mixture of air, edema, and extravasated RBC (heart failure)
-HF

-Cerebral edema: localized or generalized; narrowed sulci and distended gyri, compressed by skull – herniation may occur

-ANASARCA - general swelling of the whole body, can occur when tissues of the body retain too much fluid

Question 7

transudate vs exudate

Answer 7

-Transudate
-results from disturbance of Starling forces
-protein content < 3 g/dl, LDH LOW

-Exudate
-results from damage to the capillary wall
-protein content > 3 g/dl, LDH HIGH

Question 8

pulmonary edema

Answer 8

-pulmonary capillary pressure exceeds plasma colloid osmotic pressure
-HF

Question 9

heart failure

Answer 9

-Heart failure cells are hemosiderin laden macrophages (broken down blood)
-in the lungs
-Blood escapes into the alveolar space because chronic congestion causes the thin walled alveolar capillaries to burst.

Question 10

thrombosis

Answer 10

Pathologic blood !clot within blood vessels or within! chambers of the heart

Question 11

hemorrhage

Answer 11

Excessive bleeding when hemostatic mechanisms are blunted, insufficient or defective

-EXTRAVASATION beyond vessel
-HEMATOMA (implies MASS effect)
-PETECHIAE (1-2 mm) (PLATELETS)
-PURPURA <1cm
-ECCHYMOSES >1cm (BRUISE)
-HEMO-: -thorax, -pericardium, -peritoneum, -arthrosis

Question 12

summary

Answer 12

-PT and PTT are prolonged in liver failure

Question 13

disseminated intravascular coagulation

Answer 13

-excessive activation of coagulation and formation of thrombi
-consumptive coagulopathy - platelets and factors are being consumed to make microthrombi

-tissue hypoxia and infarction caused by microthrombi
-hemorrhage- lack of factors and activation of fibrinolytic mechanisms

-2ndary- acquired from different conditions!!!!!
-MC associated with obstetric complications, malignant neoplasms, sepsis, and major trauma

-microangiopathic hemolytic anemia!!!!
-RBCs break up (become schistocytes) and burst when trying to get through all the clots -> anemia, thrombocytopenia
-Prolonged PT / PTT

Question 14

virchow triad in thrombosis

Answer 14

-Endothelial integrity most important factor

-3 major risk factors for thrombosis: virchows
-1. Endothelial Injury
-Atherosclerosis / Hypercholesterolemia / Inflammation
-HTN / Vasculitis / Diabetes
-Toxins (Cigarette smoke) / Elevated Homocysteine

-2. Abnormal Blood Flow
-Stasis / Turbulence

-3. Hypercoagulable State
-Primary (genetic) or Secondary (acquired) disorders
-pregnancy, abnormal blood flow

Question 15

hypercoagulability

Answer 15

-venous thrombosis - primary (genetic) and secondary (acquired) disorders

-Primary include:
-Factor V Leiden (common)
-Prothrombin gene mutation (common)
-Classically present with recurrent DVTs or DVT at young age (adolescence or early adulthood)

-Acquired
-Prolonged bed rest or immobilization
-MI 
-Afib 
-Tissue damage (surgery, fracture, burns)
-Cancer (TROUSSEAU syndrome, i.e., migratory thrombophlebitis)- mucin from some cancers trigger coagulation
-prosethetic cardiac valves

Question 16

pathology of thrombosis

Answer 16

-antemortem clots- gross and microscopic lines of Zahn -> pale platelet and fibrin deposits alternating with darker red cell–rich layers

-postmortem clots- bland, non-laminated

-Postmortem clots - gelatinous with dark-red dependent portion (red cells settled by gravity) and yellow “chicken fat” upper portion

Question 17

fate of thrombus

Answer 17

-Propagation- thrombi accumulate additional platelets and fibrin

-Embolization

-Dissolution: fibrinolysis

-Organization and recanalization:
-forms new vessels (holes) in the vessel for blood to flow there

Question 18

pathology of thrombosis

Answer 18

-Venous thrombi - painful congestion and edema distal to obstruction, may embolize to lungs
-Arterial thrombi - infarctions
-Arterial or cardiac thrombi- occur at sites of turbulence or endothelial injury
-venous thrombi- occur at sites of stasis
-arterial systemic emboli- 80% cardiac origin, 20% aorta

Question 19

arterial and cardiac thrombosis

Answer 19

-Atherosclerosis: major cause of arterial thromboses due to loss of endothelial integrity and abnormal blood flow
-Myocardial infarction can predispose to cardiac mural thrombi by causing dyskinetic myocardial contraction and endocardial injury
-Both cardiac and aortic mural thrombi prone to embolization to any tissue but especially brain, kidneys, and spleen

Question 20

pulmonary embolism

Answer 20

-Originate from DVT (95%); MC thromboembolic disease

-go to right heart and “slam” into pulmonary vasculature; depending on embolus size can:
-occlude main pulmonary artery
-straddle pulmonary artery bifurcation (saddle embolus), or
-pass into smaller, branching arteries
-sudden death

-Most pulmonary emboli (60% to 80%) small and clinically silent

-obstruct 60% or more: sudden death, acute right heart failure (cor pulmonale), or cardiovascular collapse

-vascular rupture: pulmonary hemorrhage – NOT pulmonary infarction (2 supply)
-obstruction of small end-arteriolar pulmonary branches: often results in hemorrhage or infarction
-!Multiple emboli over time may cause pulmonary hypertension and right ventricular failure

Question 21

infarction

Answer 21

-An area of necrosis secondary to decreased blood flow
-HEMORRHAGIC vs. ANEMIC

-RED (hemorrhagic) vs. WHITE (anemic)
-END ARTERIES vs. NO END ARTERIES

-ACUTE -> ORGANIZATION -> FIBROSIS

Question 22

shock

Answer 22

-systemic tissue hypoperfusion from low CO and/or reduced circulation

-Major types of shock:
-cardiogenic (MI) - myocardial pump failure, ventricular arrhythmias, cardiac tamponade, outflow obstruction (pulmonary embolism)

-hypovolemic (e.g., blood loss)- low CO due to low blood volume (massive hemorrhage or fluid loss from severe burns, severe vomiting or diarrhea)

-septic (e.g., infections)
-gram negative
-Less common
-spinal cord injury ( neurogenic shock ), or an IgE-mediated hypersensitivity reaction (anaphylactic shock)
-acute vasodilation -> pooling -> hypotension -> hypoperfusion
-DIC

-Shock of any form can lead to inadequate tissue perfusion and hypoxic tissue injury; may be fatal

Question 23

shock: clinical stages: irreversible stage

Answer 23

Irreversible stage: cellular and tissue injury so severe that even if hemodynamic defects are corrected, survival is not possible
-necrosis
-sepsis- giving antibiotics will release bacterial toxins

Question 24

shock pathology

Answer 24

-MULTIPLE ORGAN FAILURE
-SUBENDOCARDIAL HEMORRHAGE
-ACUTE TUBULAR NECROSIS
-DAD (Diffuse Alveolar Damage, lung)
-GI MUCOSAL HEMORRHAGES
-LIVER NECROSIS
-DIC

Question 25

clinical progression of shock symptoms

Answer 25

-Hypotension ->
-Tachycardia ->
-Tachypnea ->
-Warm skin -> Cool skin -> Cyanosis
-Renal insufficiency->
-Obtunded mental status - depressed level of consciousness; cannot be fully aroused
-Death