Heme Flashcards
(64 cards)
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
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.
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
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
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
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
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
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
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
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
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
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
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)
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
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
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
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
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
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
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
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
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
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
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
25
Hereditary Spherocytosis
| - caused by
- problem between ankyrin and spectrin
26
RBC shapes and meaning
- Howell Jolly Bodies
- Heinz body
- Basophilic stippling
- Tear drop cell
- Target cell
- Poikilocyte
- schistocyte
- burr cell
- pappenheimer
- cabots ring
- 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
Paroxsymal Nocturnal Hemoglobinuria
- what is it
- leads to
- sxs
- dx
- 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
Macrocytic anemia
- MCV
- caused by
- if RDW normal
- over 100
- B12 (has neuro sxs) or folate deficiency (no neuro sxs)
- drugs, EtOH, liver disease
29
Thrombocytopenia
- what is it
- caused by
- signs
- most common causes
- heparin induced throbocytopenia
- 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
Hypercoagulable Dx
- Anti-thombrin 3 def
- Protein C def
- Protein S def
- Factor V leiden
- presentation
- AD, decrease in anti-thrombin 3 -> thrombin cannot be inhibited
-
-
- AD; abnrml factor V leiden cant be turned off
- arterial and venous thrombosis
31
Growth of blood vessels
- VEGF
- FGF
- stimulates angiogenesis
| - promotes endothelial proliferation, migration and differentuation, important in hematopoesis and wound repair
32
Anatomy of artery
- adventitia
- tunica media
- intima
- 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
Arterioles
- maintain
- contain most
- how
- dilation
- chronic hypertension
- malignant hypertension
- 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
Capillaries
- importance
- continuous
- fenestrated
- sinusoidal
- smooth muscle
- 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
Vascular networks
- parallel: type; resistance; calculation
- series: examples, resistance, calculation
- 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
Changes in diameter
- small arteries
- large vessels
- 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
Neuro Control of arterioles
- under control of
- how to dilate
- sympathetics, constricted w/ alpha-1 (IP3/DAG)
| - 90% of the time just turning down alpha 1 but can also use Beta 1
38
Types of pressure on inside of vessel
- linear
- transmural
- what happens as vessel narrows
- straight forward
- pushing outward against vessel wall
- velocity increases, flow decrease, resistance increases, BP increases
39
Capillary forces
- hydrostatic high, oncotic low
- hydrostatic = osmostic
- hydrostatic low, oncotic high
- 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
Transudate
- what is it
- how did it get out vasc
- causes for hydro
- causes for oncotic
- 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
Exudate
- made up of
- purulent
- fibrinous
- serous
- malignant
- catarrhal
- 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
Bilateral vs Unilateral LE edema
- bilateral
- unilateral
- heart, kidney, liver failure
| - vasc insuff, DVT
43
Ascites
- what is it
- type
- SAAG: equation, high, low
- gradient 1.2-2.5
- gradient > 2.5
- gradient <1.1
- 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
Blood flow resistance
| - equation
- length times viscosity / diameter ^4
45
Arterio-nevous O2 diff
- what is it
- increases with
- rest
- exercise
- after eating
- studying
- decreased
- % 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
Fistula
- congenital
- caused
- diseases
- PDA
- renal dialysis
- von hippel lindau, osler weber
47
Anastamoses
- what is it
- importance
- location
- 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
Vericose Veins
- why do they occur
- smaller v
- caused by
- what happens when it can no longer accomodate
- look like
- 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
Neuro Control of V
- under control of
- usually
- constricted: how, why?
- parasymapthetics
- dilated
- w/ alpha 1, only happens w/ blood loss
50
vasculitis
- most common cause of death
- sxs
- wht happens
- IgA nephropathies
- 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
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
- 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
DIC
- what is it
- labs
- management
- 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
Thrombotic Thrombocytopenia Purpura
- what is it
- sxs
- managmenet
- 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
Ankylosing spondylitis
- HLA
- start w/
- xray
- + Schoerber test
- B27
- sacroiliitis
- bamboo spine
- aortitis -> lead to dissection, aortic regurg murmur
55
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
- 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
Juvenile RA:
- sxs
- Oligoarticular
- Systemic
- Polyarticular
- feltys disease
- bechets
- 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
Schogrens
- sxs
- antibodies
- diff from sicca syndroms
- dry eye, dry mouth
- anti-ro (SSA), anti-LA (SSB)
- no arthritis and no antibodies
58
Serum Sickness
- what is it
- when
- vaccine
- measles like illness
- 2 weeks after vaccination
- MMR
59
Subacute bacterial endocarditis
- location
- caused by
- dx
- tx
- 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
Systemis Lupus Erythematosus
- antibodies
- anticardiolipin: what does it do; sxs; false positive on
- dsDNA
- COD
- sxs
- tx
- renal dx, tramtrack appearance
- 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
Cyro-globulinemia
- what is it
- when, mediated by
- infections
- antibody deposition affect any vessel in body
- on ly with cold, igM
- influenza, adenovirus, mycoplasma, hep B, EBV
62
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
- 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
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
- 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
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
- 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
