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Boards II > Heme > Flashcards

Heme Flashcards

1
Q

Anti- coagulants

  • Heparin: MOA; indication; HITT: what is it, sxs, tx; unfractionated: what does it do, measure; low molecular weight: significance, metabolism, other; administration
  • warfain: MOA, indication, advesrse affect
A
  • binds to anti-thrombin 3 and makes it work better -> inhibits factor 2, 9, 10, 11, 12; prevent DVT and PE; immune reaction against heparin that then atsrts acting on platelets and causes them to stick to eachother -> pt presents w/ clotting because -> use argatriban; inhibits factor 10 and 2 and causes more bleeding complications, PTT; smaller molecule that inhibits Factor 10a more than 2, so less bleeding complication, through kidney so need to monitor pts w/ renal dx, based on weight so hard to give to obese and pregnant pts bc need higher dose; given as injection on abdominal wall and with HITT reaction cause cause necrosis at injection site
  • atagonizes vit k -> onterferes with 2, 7, 9, 10, C and S; prevention of DVT; skin necrosis bc it depletes protein C -> bridge w/ hepain
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2
Q

Anti thrombotics

  • Aspirin: MOA; side effects;
  • Ticlopidine: MOA, indication, adverse effect
  • Clopidogrel: MOA, indication, adverse effect, dosage normally and after MI
  • Cilostazol: MOA, indication; side effect
  • Dipyridamole: MOA, indication, side effects
A
  • inhibits COX enzymes; at low doses it will inhibit only COX1 -> anti-thrombotic, at high doses it will inhibit COX 1 and 2 -> anti-thrombotic, analgesic, anti pyretic; GI ulcer -> bc of decrease in prostaglandin
  • irreversible blockage of platelet binding to fibrinogen, preventing activation of platelets; decrease stroke risk in those who cannot tolerate baby aspirin; increase risk of bleeding, neutropenia
  • Blocks platelet aggregation by inhibiting ADP receptor; decrease risk stroke, MI; bleeding and potential for hemorrhage (needs to be stopped before surgery); 75 mg 1x a day, but when placing stent give big dose during surgery because will immediately stop platelet adherence
  • inhibits phosphodiesterase 3 -> increase cAMP -> causes SM relaxation -> vasodilation; intermittent claudication and PAD; palpitation, headache
  • inhibits phosphodiesterase; w/ aspirin will decrease platelet life span and w/ warfarin will prevent emboli on artifical valves; will also increase adenosine which is potenet vasodilator -> exacerbates angina because will take blood away from some vessels that have calusdication and need higher and stronger flow.
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3
Q

Thrombolytics

  • streptokinase: indications; moa
  • urokinase: MOA
  • tissue plasminogen activator: indication; MOA
  • alteplase: indication; MOA
A
  • STEMI, only if dealing w/ ischemic tissue, also good for PE, DVT, and peripheral artery thrombosis; activated plasminogen into plasmin
  • same as streptokinase
  • reperfusion of occluded arteries; binds to fibrin and activates fibrin bound plasminogen into plasmin
  • acute MI, or stroke; MOA is same as TPA
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4
Q

GpIIb/IIIa Inhibitors

  • abciximab
  • ebtifibatibe
  • tirofiban
A
  • Fab of murine monoclonal antibody to human GpIIb/IIIa
  • cyclic peptide snake venom
  • non peptide antagonist
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5
Q

Hematopoeitic Drigs

  • erythropoeitin alpha: MOA, indications
  • filgrastrim: MOA, indications
  • sargramostim: indication, MOA
  • oprelvekin: MOA, indications
A
  • recombinant EPO; stimulates erythropoeisis; anemia w/ chronic renal failure
  • human recombinant granulocyte colony stimulating factor (stimulates production of PMN); when using myelosuppressive drugs
  • accelerates bone marrow replenishment when patient undergoes BM transplant; will stimulate all blood cell lines except for RBC and platelet
  • stimulates production of platelets; after chemo to increase platelet count
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6
Q

Erythrocyte Sedimentation Rate

  • what is it
  • stimulated by
  • high
  • low
A
  • non specific marker of inflammation
  • high levels of circulating fibrinogen
  • AI, CA, infection or pregnant
  • polycythemia, liver dx, sickle cell
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7
Q

Heme Synthesis

  • starts w
  • rate limiting enzyme
  • AA used
  • vitamin needed
  • Ferrochelatase
  • Ferrous vs ferric
A
  • Succinyl CoA
  • aminolevulinic acid synthase
  • glycine
  • B6
  • adds Fe2+ into porphyrin rings to make it heme; occurs in mito
  • ferrous (2+) bins to heme but ferric (3+) will not; ferric is what is absorbed in gut and is cannot be changed into ferrous bc of histidine
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8
Q

CO2 and Chloride Shift

- how is CO2 carrried

A
  • carbamate and bicarb; converted to bicarb in the RBC but then diffuses into plasma and Cl goes into the RBC
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9
Q

Types of anemia

  • iron deficiency: labs
  • sickle cell and thalassemia labs
  • lead poisoning and sideroblastic labs
  • chronic dx
  • AI hemolysis
  • hereditary spherocytosis
  • elliptocytosis
  • G6PDH def
  • Megaloblastic anemia
A
  • MCV lower than 80, ferritin is low
  • low MCV, normal ferritin, + Hb electrophoresis
  • low MCV, normal ferritin, - Hb electrophoresis
  • MCV 80-100; reticulocyte count normal
  • MCV 80-100; reticulocyte count normal
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10
Q

Types of anemia

  • iron deficiency: labs
  • sickle cell and thalassemia labs
  • lead poisoning and sideroblastic labs
  • chronic dx labs
  • AI hemolysis labs
  • hereditary spherocytosis and elliptocytosis labs
  • Megaloblastic anemia
A
  • MCV lower than 80, ferritin is low
  • low MCV, normal ferritin, + Hb electrophoresis
  • low MCV, normal ferritin, - Hb electrophoresis
  • MCV 80-100; reticulocyte count normal
  • MCV 80-100; reticulocyte count high, coombs test +
  • MCV 80-100; reticulocyte count high, coombs test -, Hb electrophoresis normal
  • MCV greater than 100, low B12 or folate
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11
Q

Iron deficiency anemia

  • iron and ferritin
  • TIBC
  • cause in children and young adults
  • cause in 20-40 yr old
  • cause in child bearing women
  • tx
A
  • decreased
  • increased
  • inadequate intake
  • ulcers and hemmorrhoids
  • period
  • ferrous sulfate 325 mg 2-3x a day
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12
Q

Sickle Cell anemia

  • caused by
  • type mutation
  • age
  • what happens
  • dactylitis
  • what causes anemia
  • crisis
  • vaso occlussive crisis
  • sxs
  • aplastic crisis
  • management: other
  • management: hydroxy urea
  • management: life time folic, why?
  • management: antibioitics, why?
  • management: cure
  • senicapoc: what is it, how does it work
  • avoid: hypoxic situations
  • protective against
A
  • qualitative problem bc valine is substituted for glutamic cid in beta chain
  • AR
  • 6 mnths
  • hypoxia causes sickling -> vaso occlusion
  • fingers and toes experience RBC sickling leading to inflammation and extreme
  • hemolysis bc sickled RBC only last 10 days instead of 120 days
  • complications that occur bc of sickling
  • CVA, pulm infarction, splenic sequestration (can cause auto splenectomy), priapism (prolonged and painful erection)
  • exertional dyspnea, recurrent abd pain, bone pain
  • check reticulocyte and if it is not elevated then the patient is unable to make new RBC, usually caused by Parvo
  • oxygen, exchange transfusion
  • increase NO -> increase cGMP -> activates gamma globulin chain synthesis -> increase in HbF
  • lifetime folic -> bc constantly having to make reticulocytes bc of constant lysis of RBC
  • penicillen for meds
  • BM transplant
  • gardos channel blocker; usually allows K to leave RBC and water will follow causing dehydration of cell and leading to sickling; so we block channel
  • deep sea diving, airplane decompression, smoke inhalation, mountain climbing
  • malaria, infects and replicates in RBC; better to have sickle cell trait (hetero) because will have tolerance to infection but did not have sickle cell problems
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13
Q

Hemoglobin C dx

  • mutation
  • causes
  • sxs
  • sickling?
  • management
A
  • lysine replaces glutamic acid on b chain
  • leads to decrease in mobility
  • have mild hemolytic anemia, sporadic episodes of MS pain, bili rubin stones bc of hemolysis
  • blood cells do not sickle
  • eye exams (bc can have retinopathy)
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14
Q

Hemoglobin Electrophoresis

  • HbA vs HbS
  • HbA vs HbC
A
  • HbS replaced negative charged glutamic acid w/ non polar valine so HbS will not move as far down the electrode as normal HbA
  • HbC replaced negative charged glutamic acid w/ positively charged so HbC will not move as far down the electrode as normal HbA or HbS
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15
Q

Thalassemias

  • inhertiance
  • ethnicity
  • betha thal
  • alpha thal
A
  • AR, mutation produces defective mRNA
  • mediterranean
  • beta chain not produced correctly
  • alpha chain not produced correctly
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16
Q

Beta Thal

  • coded by
  • minor
  • major
  • thalssemia intermedia
  • tx of major
A
  • 2 genes
  • asymptomatic; mild hypochromic microcytic anemia w/ increased HbF, A2 and target cells
  • both genes are missing; only see Hgb A2 and Hgb F on electrophoresis
  • mutation of kozak sequence, causing 30% decrease in production of beta chains
  • chronic transfusion, iron chelation, BM transplant
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17
Q

Alpha Thal

  • coded by
  • asymptomatic
  • 2 genes missing sxs
  • 3 genes missing sxs: Hgb Bart; Hgb H
  • alpha thal major: what is it, leads to, prognosis
  • tx for major
A
  • 4 genes
  • 1 gene missing
  • sxs only when active
  • sxs all the time; can produce Hgb Bart (hemogloin with 4 gamma chains) and has high affinity for O2 and will not deliver O2 to tissues; Hgb H is 4 beta chains and has high affinity for O2, no delivery to tissues
  • all 4 genes missing; cannot make hemoglobin; hydrops fatalis -> baby dies of HF
  • chronic blood transfusion, iron chelation (bc of blood transfusions), spleenectomy, BM transplant
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18
Q

Extramedullary Hematopoesis

  • what is it
  • description
A
  • liver and spleen help make RBC bc of chronic hemolytic anemia
  • enlargement of flat bones, skull or ribs
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19
Q

Blood Transfusions for thalassemia

  • given
  • 1 unit of packed RBC increase
  • why packed RBC
  • rule of thumb
  • cyroprecipitate contains
  • transfusions reactions: anyphylaxis - what is it, sxs, management
  • transfusions reactions: febrile reaction - what is it, sxs, management
  • transfusions reactions: ABO reaction - what is it, sxs, management
A
  • when symptomatic
  • Hb by 1 and HcT by 3
  • only RBC, no plasma; whole blood is used for trauma
  • for every 2 units of pRBC, give 1 unit FFP (because diluting out all other blood products including clotting factors and will cause bleeding)
  • factor 8, vWF, and fibrinogen
  • caused by recipient not having IgA and blood products having IgA, causing recipients IgG to go off; flushing, swelling, wheezing; stop transfusion and give epi, next time filter blood for IgA
  • fever after transfusion bc of white cell antigens -> this is why cells are washed; give acetaminophen
  • RBC lysed, Fever and low back pain; stop transfusion, intubate, supportive care
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20
Q

Iron Overload

  • hemosiderosis
  • hemochromatosis: what is it, sxs, primary vs secondary,
A
  • deposition of hemosiderin in macrophages w/o tissue damage
  • iron overload in parenchymal tissue; restrictive cardiomyopathy, arthritis, testicular failure, discoloration of skin, joint and bone pain (psuedogout); auto recessive, chronic transfussion; phlebtomy and deferoxamine
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21
Q

Lead poisoning

  • what does it do
  • sxs
  • stored
  • sources
  • management: dimercaprol, EDTA, succimer
A
  • inhibit enzymes alpha aminolevulinic acid dehydratase and ferrochelatase -> cannot add iron to rings
  • basophilic stiffling -> porphyrin ring stuck to incise of RBC wall
  • abd pain and constipation, HA, lead line (blue pigmentation at gum and tooth lin), short term memory loss, loss appetite, irritability, depression
  • blood, soft tissue, bones
  • lead paint chips (taste sweet), chemical processing, spray pain, repairing radiators, miners
  • chelation: dimercaprol -> use in addition to EDTA bc can cross BBB; EDTA -> binds 2+ ions, give w/ calcium, does not cause BBB so does not help w/ encephalopathy, succimer -> water soluble, oral agent, recommended for children with lead level greater than 45
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22
Q

Anemia of Chronic dx

  • caused by
  • TIBC
  • ferritin
  • what happens
  • anemia of renal failure - cytokines and effect
  • chronic dx
A
  • chronic infectious or inflammatory process
  • decreased
  • increased
  • iron is stored in increased amount in marrow macrophages
  • IL beta, IL6, gamma IFN and TNF alpha -> inhibit EPO and erythroyte proliferation
  • macrophages begin to phago RBCs and increase in hepcidin to inhibit iron release
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23
Q

Coombs test

  • when is it done
  • direct: how
  • indirect: how, why?
A
  • MCV normal, reticulcyte count increased
  • antibodies are attached to antigen on RBC, so add coombs reagent which bind to antibodies on RBC and will cause RBC to agglutinate
  • pt will have antibodies in serum -> add reagent RBC, add combs reagent -> agglutination; used as prenatal or pre- blood transfusion test
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24
Q

AI hemo anemia

  • what is it
  • types
  • labs
  • cold
  • warm
A
  • premature RBC destruction that leads to anemia when BM cant keep up
  • intravascular (RBC lyse in circulation), extravascular (RBC phago by macrophages in liver or spleen)
  • reticulocytosis (BM trying to compensate), increased LDH, reduced plasma haptoglobin (protein bound to hb when loose in blood)
  • IgM mediated, only in cold temp, hemolysis through MAC
  • IgG mediated, body temp, causes opsonization and phago by macrophages
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25
Q

Hereditary Spherocytosis

- caused by

A
  • problem between ankyrin and spectrin
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26
Q

RBC shapes and meaning

  • Howell Jolly Bodies
  • Heinz body
  • Basophilic stippling
  • Tear drop cell
  • Target cell
  • Poikilocyte
  • schistocyte
  • burr cell
  • pappenheimer
  • cabots ring
A
  • nuclear remnant in RBC
  • G6PD deficiciency
  • porphyrin ring stuck inside RBC; lead poisoning
  • hemolytic anemia or CA
  • missing hb; thalassemia, and liver dx
  • cells in diff stages of development
  • fragmented RBC, mechanical cell
  • uremia
  • inclusion body w/ ferritin inside; sideroblastic and sickle cell
  • remnant of mitotic spindle; lead and pernicious anemia
27
Q

Paroxsymal Nocturnal Hemoglobinuria

  • what is it
  • leads to
  • sxs
  • dx
A
  • acquired mutation of PIGA gene, coding for GPI anchor which normally protects RBC from complement
  • complement mediated RBC lysis
  • hemoglobinuria with dark urine throughout night
  • hams test -> check fragility of RBC when placed in acid
28
Q

Macrocytic anemia

  • MCV
  • caused by
  • if RDW normal
A
  • over 100
  • B12 (has neuro sxs) or folate deficiency (no neuro sxs)
  • drugs, EtOH, liver disease
29
Q

Thrombocytopenia

  • what is it
  • caused by
  • signs
  • most common causes
  • heparin induced throbocytopenia
A
  • low platelet count
  • elevated bleeding time (50K), dangerous bleeding (20k), bleeding into CNS (10K)
  • stem cell failure, splenic sequestration, increased destruction of platelets
  • idiopathic, thrombotic throbocytopenic purpura (lack of activity in the ADAMTS13 enzyme, VWF is not chopped up, platelets adhere easier, causes thrombosis), hemolytic, uremic sxs: caused by shigella toxin; DIC; drugs (heparin, sulfonamide, valproic acid)
  • pt produces antibodies against heparin which cross react with platelet factor 4 causes platelet destruction; as platelet count drops will get paradoxical thrombosis instead of bleeding; stop heparin and give direct thrombin inhibitor
30
Q

Hypercoagulable Dx

  • Anti-thombrin 3 def
  • Protein C def
  • Protein S def
  • Factor V leiden
  • presentation
A
  • AD, decrease in anti-thrombin 3 -> thrombin cannot be inhibited
  • -
  • AD; abnrml factor V leiden cant be turned off
  • arterial and venous thrombosis
31
Q

Growth of blood vessels

  • VEGF
  • FGF
A
  • stimulates angiogenesis

- promotes endothelial proliferation, migration and differentuation, important in hematopoesis and wound repair

32
Q

Anatomy of artery

  • adventitia
  • tunica media
  • intima
A
  • contains vaso vasorum (blood supply to adventita and 2/3 media)
  • usually has elastin but under stress can produce collagen
  • supplied by blood through diffusion,
33
Q

Arterioles

  • maintain
  • contain most
  • how
  • dilation
  • chronic hypertension
  • malignant hypertension
A
  • BP
  • SM by surface area
  • vasoconstrict and dilate
  • Beta 2 receptors
  • lead to reactive vasoconstriction -> hyaline arteriole sclerosis because increase in pressure causing damage to artery
  • hyperplastic arteriole sclerosis -> onion skinning
34
Q

Capillaries

  • importance
  • continuous
  • fenestrated
  • sinusoidal
  • smooth muscle
A
  • gas and nutrient exchange
  • go straight into vein
  • endo cells have holes so more things can diffuse
  • gaps between cells so that bigger molecules can diffuse in and out
  • none
35
Q

Vascular networks

  • parallel: type; resistance; calculation
  • series: examples, resistance, calculation
A
  • artery to capillaries to v; does not produce as much resistance; total resistance = 1 / (1/R1 + 1/R2 + 1/R3)
  • 1 artery breaking into arterioles and then giving rise to capillaries, GI and hepatic circulation bc mesenteric v go into hepatic v; higher, total resistance = R1+ R2+ R3 +R4
36
Q

Changes in diameter

  • small arteries
  • large vessels
A
  • changes in diameter and resistance of small a have greatest effect on vascular resistance bc make up 70% of total resistance in most organs
    would have to compress by more than 50% in order to have significant effect on blood flow
37
Q

Neuro Control of arterioles

  • under control of
  • how to dilate
A
  • sympathetics, constricted w/ alpha-1 (IP3/DAG)

- 90% of the time just turning down alpha 1 but can also use Beta 1

38
Q

Types of pressure on inside of vessel

  • linear
  • transmural
  • what happens as vessel narrows
A
  • straight forward
  • pushing outward against vessel wall
  • velocity increases, flow decrease, resistance increases, BP increases
39
Q

Capillary forces

  • hydrostatic high, oncotic low
  • hydrostatic = osmostic
  • hydrostatic low, oncotic high
A
  • on arterial side, hydrostatic is greater than osmotic -> fluid pushed out; oncotic pressure low because lots of fluid so not pulling
  • no movement
  • osmotic higher than hydrostatic so it is pushed back in; oncotic pressure high because not enough fluid and proteins attract positive charge of water
40
Q

Transudate

  • what is it
  • how did it get out vasc
  • causes for hydro
  • causes for oncotic
A
  • mostly water
  • decreased oncotic pressure or increase hydrostatic pressure in vessel
  • kindey failure, and heart failure
  • kwashikor, cirrhosis, nephrotic syndrome (losing too much protein from kidneys), menientieres
41
Q

Exudate

  • made up of
  • purulent
  • fibrinous
  • serous
  • malignant
  • catarrhal
A
  • protein and fluid
  • pus, live and dead tissue,
  • AI and rehumatic disorder
  • less protein, clear or slightly yellow… indicates inflammation or normal healing
  • has CA cells
  • found in nose and throat and has lots of mucus
42
Q

Bilateral vs Unilateral LE edema

  • bilateral
  • unilateral
A
  • heart, kidney, liver failure

- vasc insuff, DVT

43
Q

Ascites

  • what is it
  • type
  • SAAG: equation, high, low
  • gradient 1.2-2.5
  • gradient > 2.5
  • gradient <1.1
A
  • fluid accumulation in abd cavity
  • transudative or exudative
  • [protein] serum - [protein]
  • cirrhosis
  • heart failure or budd chiari
  • not due to increased hydrostatic pressure bs protein and fluis have same amount of protein -> nephrotic, TB or CA
44
Q

Blood flow resistance

- equation

A
  • length times viscosity / diameter ^4
45
Q

Arterio-nevous O2 diff

  • what is it
  • increases with
  • rest
  • exercise
  • after eating
  • studying
  • decreased
A
  • % O2 extracted by tissues
  • when tissue is metabolically active or decreased flow
  • heart
  • muscle
  • GI
  • brain
  • less metabolic activity, flow is increased or fistula
46
Q

Fistula

  • congenital
  • caused
  • diseases
A
  • PDA
  • renal dialysis
  • von hippel lindau, osler weber
47
Q

Anastamoses

  • what is it
  • importance
  • location
A
  • no capillaries, just goes straight from A to V
  • shunt blood away from non-essential structures at times of need
  • lips, ears, nose, finger/toes
48
Q

Vericose Veins

  • why do they occur
  • smaller v
  • caused by
  • what happens when it can no longer accomodate
  • look like
A
  • valves do not function properly in larger v
  • spider v
  • DVT, pushed apart by increased standing
  • blood will leak out and cause skin to turn purple
  • dilated, tortous veins
49
Q

Neuro Control of V

  • under control of
  • usually
  • constricted: how, why?
A
  • parasymapthetics
  • dilated
  • w/ alpha 1, only happens w/ blood loss
50
Q

vasculitis

  • most common cause of death
  • sxs
  • wht happens
  • IgA nephropathies
A
  • heart failure, bc inflammation will attack hear vessels
  • petechiae, purpura, ecchymoses
  • PMNs comin, t cells and macophages follow at 4 days, fibroblasts come in at end to scar up
  • Berger and Henoch Schonlein
51
Q

Vasculitis

  • Berger Dx (NO U): time frame, presentatoin, management
  • Buergers: what is it, associated w/, epi, sxs, raynauds phenomenon
  • Henoch- scholein purpura: sxs; epi; caused by; leukocytoclastic vasculitis
  • Diabetes
  • Syphylis
  • Kawasaki: type disorder, epi, size, hx of, acute sxs, sequalae/ aubacute sxs; mgmnt
  • temporal arteritis: epi, histo, sxs
  • polyarteritis nodosa: epi, size, associated with, pANCA, sxs
  • leukocytoclastic vasculitis: caused by, sxs
A
  • 2 wks after common cold, present with hematuria, follow them and if get worse treat renal failure, if better just continue to watch
  • thromboangitis obliterans, strong, progressive and recurring inflammation and thrombosis of digital vessels; association w/ tobacco use; young, caucasian; gangrene; sensitivity to cold
  • raised rash (starts at waist and moves down), arthritis (ankles, knees, elbows), abd pain (GI hemmorrhage bc of intussusception); in child; antigen exposure causes IgA to be made and it implants in blood vessel wall and in renal mesangium; PMNs destroying blood vessel wall bc of IgA implantation
  • increased glucose causes increase viscocity -> increased inflammation AND excess glucose turns into sorbitol by enzyme aldol reductase which accumulates in nerves and causes neuropathy; symmetric, distal neuropathy (glove and stocking)
  • Leads to hyperplastic thickening of aortic walls -> oschemia to outer 2/3 of aorta -> aortic aneurysm
  • AI disorder; children; medium sized arteries; hx of viral infection; fever, myocarditis, conjunctivitis, strawberry tongue; coronary a aneurysm leading to MI, generalized desquamation rash; IV immunoglobulin, high dose aspirin, immunization for varicella and inflammation
  • older females; multi-nucleated giant cells adjacent to fragmented internal elastic lamina; headache, jaw pain, visual problems (steroids then biopsy)
  • middle aged men; fibrinoid necrosis of media of medium sized vessels; associated with hep B; pANCA neg; neuropathy, abd pain, melena, weight loss, malaise, fever
  • immun complex deposition because of drug allergy with neutrophil chemotaxis and damage -> give rise to palpable purpura
52
Q

DIC

  • what is it
  • labs
  • management
A
  • activation of clotting cascade secondary to an insult (pancreatitis, gram - sepsis, burns) and burn through platelets so begin to bleed from everywhere
  • PT/ PTT elevated, elevated D-dimers
  • Fresh frozen plasma
53
Q

Thrombotic Thrombocytopenia Purpura

  • what is it
  • sxs
  • managmenet
A
  • caused by aunto-antibody toward ADAMTS13, vWF not split, platelets start clotting
  • fever, anemia, thrombocytopenia, renal involvnement neuro sxs
  • plasmapharesis -> filter out antibodies and FFP
54
Q

Ankylosing spondylitis

  • HLA
  • start w/
  • xray
    • Schoerber test
A
  • B27
  • sacroiliitis
  • bamboo spine
  • aortitis -> lead to dissection, aortic regurg murmur
55
Q

Collagen Vascular dx

  • CREST: what is it, sxs; antibody
  • Scleroderma: severe form of, histo, antibody
  • Progressive systemic sclerosis: what is it; antibody
  • Mixed CT disease: sxs, antibody
A
  • mildest form of scleoderma; calcinosis (dystrophic calcificiation), raynauds ( spasm of vessel of fingers and toes when cold -> give Ca channel blocker), esophageal dysmotility, sclerodactily: fingers and toes develop skin thickening; anti centromere antibody
  • more severe form of CREST , onion skining of kidney bc of HTN; anti-SCL 70 (anti-topo 1)
  • severe form of sclerosis that lead to scarring of liver and other organs, anti-SCL70
  • can have raynauds, arthralgia, sinusitis, esophegeal dysmotility; anti- ribnuclear protein antibody
56
Q

Juvenile RA:

  • sxs
  • Oligoarticular
  • Systemic
  • Polyarticular
  • feltys disease
  • bechets
A
  • joint pain, joint swelling, fever;
  • 1-4 months in first 6 months and 5 or fewer joints after first 6 months; higher incidence of ANA, non symmetrical
  • No limit to joint involvement, slamon pink rash and fever comes and goes with HSM
  • Involvement of 4 or more joints after 6 months w/ illness
  • RA + leukopenia + spleenomegaly
  • RA +G I/GU ulcers, erythema nodosa + PAD
  • RA + Xerophthalmia + Xerostomia
57
Q

Schogrens

  • sxs
  • antibodies
  • diff from sicca syndroms
A
  • dry eye, dry mouth
  • anti-ro (SSA), anti-LA (SSB)
  • no arthritis and no antibodies
58
Q

Serum Sickness

  • what is it
  • when
  • vaccine
A
  • measles like illness
  • 2 weeks after vaccination
  • MMR
59
Q

Subacute bacterial endocarditis

  • location
  • caused by
  • dx
  • tx
A
  • mitral valve
  • strep viridans
  • septic emboli (vegetation breaks off and end up in brain), roth spots on retina, splinter hemmorrhages, osler nodes (painful lesion on fingers and toes), janeway lesions (non-painful lesion on fingers and toes)
  • prophylaxis before dental surgery -> amoxicillin
60
Q

Systemis Lupus Erythematosus

  • antibodies
  • anticardiolipin: what does it do; sxs; false positive on
  • dsDNA
  • COD
  • sxs
  • tx
  • renal dx, tramtrack appearance
A
  • snti-SMITH, anti-dsDNA, anti-cardiolipin
  • stimulates intrinsic clotting sxs; women with mult spontaneous abortions; VDRL when testing for syphilis
  • nephrotoxic w/o response to antibody
  • only vasculitis where most common cause of death is renal failure
  • malar rash
  • cyclophosphamide
  • membranproliferative glomerulonephritis; old basement membrane, complex deposited, new basement membrane (running parallel)
61
Q

Cyro-globulinemia

  • what is it
  • when, mediated by
  • infections
A
  • antibody deposition affect any vessel in body
  • on ly with cold, igM
  • influenza, adenovirus, mycoplasma, hep B, EBV
62
Q

Aneursym

  • what is it
  • cause by
  • risk
  • sites
  • fusiform vs saccular
  • true vs false/pseudo
  • sxs
  • abd aortic aneursym: sxs, rupture, increased risk of rupture, dx, tx, complications, screening
  • periphery
  • dissection: what is it; how?; all layers; presentation of aortic dissection; stanford A vs B; dx; tx
A
  • abnormal dilation of arter to more than 1.5 normal size
  • focal weakness in vessel wall
  • smoking
  • abd aorta, femoral, popliteal
  • sides get bigger vs sac pouching out of side
  • true is all 3 layers dilating vs false with only adventitia; caused by physician such as when removing needle -> pt starts bleeding and blood gets trapped by adventita layer
  • asymptomatic -> but rupture is painful/ uncomfortable
  • pulsatile abdominal mass, ruptures is surgical emergency bc large loss of blood; larger it is the greater the risk; US to confirm and get approx size, but CT or MRI when going to operate; only tx if greater than 5.5 cm because risk of rupture higher than risk from surgery; MI, renal failure, colonic ischemia, formation of fistula between aorta and duodenum; 65 y/o w/ hx of smoking
  • most common in popliteal a, bilaterally; many also have AAA
  • tear in an artery allowing blood to flow in the layers forcing them apart; brings up endo layer and gets into media layer splitting it into inner 2/3 and outer 1/3 then flows parallel under it; dissection through all 3 leas to blood loss; severe tearing pain originates in chest and radiates to scapula; proximal, involves ascending and arch -> need surgery, type B is descending -> managed with BP meds; get urgert x-ray (widening of mediastinum) or CT (visulaize false lumen); control BP with beta blocker, then if type A go to surgery but if type B then control BP chronically
63
Q

Peripheral Vascular Dx

  • caused by
  • presents w/
  • dry gangrene: what is it; most common cause; management
  • wet gangrene: what is it; most common cause; management
  • leriche syndrome: what is it, sxs, dx, tx
A
  • atherosclerosis in LE
  • cramping like pain in LE after walking certain distance and pain is reproducible and consistent; shiny skin on LE w/o hair;
  • impaired blood flow to affected area w/ tissue discoloration, necrosis w/o infection, loss of limb; diabetes; does not need to be removed but recommend that it is
  • necrosis and infection; injury and not enough blood to heal; removal of limb, and leave open to make sure infection drains before it is closed up
  • aortoilliac insufficicency -> thigh and buttock claudication, diminished or absent femoral pulses, impotence; ABI (blood pressure at ankle/ blood pressure of arm) and duplex (triphasic -> normal, biphasic -> moderate, monophasic -> severe); lifestyle mods, cilastozol (PDE inhibitor) pentoxyfylline (causes RBC to traverse stenotic lesions easier), angioplasty
64
Q

Vessel Dx

  • venous ulcer: caused by, location, sxs; tx
  • arterial: caused by, location, sxs; tx
  • carotid vascular dx: caused by
  • subclavian steal syndrome: what is it, caused by, sxs, dx, tx
A
  • incompetent valves leading to venous HTN; ankle/calf region; painless and shallow ulcer that contains granulation tissue in an attempt to heal; compression boots/stockings
  • secondary to occlusive artery dx; dorsum of foot, toes, heels; painful; bypass surgery
  • atherosclerotic plaque at carotid bifurcation; duplex; anticoagulation to prevent thrombosis and surgery if symptomatic with 50% or mor stenosis or asymptomatic with stenosis greater than 60%,
  • Occlusion of one of the subclavian a, uses other subclavian to supply brain and then takes blood supplied to brain to bring back to subclavain on other side of claudication; atherosclerosis, takayasu arteritis; presyncope, syncope, bad circulation in hands; CT, angiogram; stenet placement

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