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272 Cards in this Set
- Front
- Back
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what is the clotting Cascade?
what are its two components? |
how you stop bleeding.
Extrinisic: something cut you=> Factor 7 Intrinsic: blood vv. pop (vasculitis, sepsis) |
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Extrinisic pathway
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something cut you=> Factor 7
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Intrinsic pathway and examples
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blood vv. pop
(vasculitis, sepsis) |
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Petechiae
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dot hemorrhage
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Papule
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palpable
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Ecchymosis
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bruise
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⇧PTT and Bleeding Time: give 2 differential dx
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VWD
SLE |
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Hemolysis: describe the LDH and haptaglobin levels
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⇧LDH
⇩Haptoglobin |
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what does bleeding Time tell you?
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tells you it's a platelet problem or a vasculitis
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where would one bleed if it is a Platelet problem
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=> bleed from skin and mucosal surface
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Clotting problem
what is increased? |
=> bleed into cavities (⇧bleeding time)
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what are the cavites you can bleed into.
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intracranial, mediastinal, pleural, pericardium, pelvis, retroperitoneum, thighs,
abdominal, skin (bruise), around umbilicus, flank |
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what can each cavity lead to when there is bleeding into it.
intracranial => mediastinal=> pleural => pericardium = > abdominal => skin=> around umbilicus=> bleeding into flank=> |
intracranial => herniation
mediastinal=> rips aorta pleural: hemoptysis => stops lungs from expanding pericardium = > tamponade abdominal =>hematemesis Dark blood: melena skin=>ecchimosis Cullen's sign: bleeding around umbilicus=> hemorrhagic pancreatitis Turner's sign: bleeding into flank=> hemorrhagic pancreatitis |
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Cullen's sign:
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bleeding around umbilicus=> hemorrhagic pancreatitis
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Turner's sign
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bleeding into flank=> hemorrhagic pancreatitis
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what is compartment Syndrome and what does it lead to?
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Tissue pressure > 30: Rhabdomyolysis ⇨ Mb ⇨ renal failure
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signs and symptoms of compartment syndrome?
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Pain w / muscle movement (first)
• Pallor • Poikylothermia: cold • Paresthesia • Pulselessness: bad prognosis (last) |
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what is virchow's triad what are these and examples
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thrombosis risk factors
1) Hypercoagulable (Ex: sepsis, trauma, amniotic fluid, cancer) 2) Stasis (Ex: A Fib, pregnancy, truck drivers, post-op) 3) Endothelial damage (Ex: vasculitis) |
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how do we measure the intrinsic Pathway
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measure PTT "The PTT is inside"
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how do we measure the extrinsic Pathway
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measure PT "PeT the dog outside"
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The Coagulation Cascade Coalesced (time)
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takes 2 hrs
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Kallikrein
when is this released? |
Released w/ inflammation ⇨ DIC
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another name for Factor 1
what is the name of its activated form? |
"Fibrogen", activated form is fibrin
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Factor 2
name and its name its activated form? |
"Prothrombin", actived form is thrombin
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Factor 7: 1/2 life
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2nd shortest half-life
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where is Factor 8 made?
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Made by endothelium (only factor not made by the liver)
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Factor 9
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"Christmas factor"
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Factor 11
what does E2 affects? is this affected by estradiol as well? |
Not increased by estrogen (E2 loves to increase Fibrinogen)
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Factor 12
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"Hageman factor"
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Factor 13
function |
Helps hold clot together
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Protein C describe its half life
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shortest half-life
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Protein S
function |
Co-factor for Protein C
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Type IV collagen (GP2b3a): function
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anchors platelet to BM,
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von Willebrand Factor: function
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1) anchors Factor 8 to platelet
2) anchors platelets to endothelium |
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Vit K
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Co-factor for γ-carboxylation
=> adds negative charges that are attracted to all that Ca+ |
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Vit K dependant factors
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Factors 2,7,9,10, Proteins C,S
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Serine Proteases
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Factors 2, 9-12
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what do platelets release?
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"5 CATs"
•5-HT •Ca2+ •ADP •TXA1 |
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5-HT: function
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=> vasoconstricts only in the brain to protect it
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TXA1: 2 functions
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=> vasoconstrict, platelet aggregation
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ADP: function
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=> energy for platelet aggregation
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Ca2+: function
what is the disadvantage of this? |
=>attracts Vit. K-dep. factors (2,7,9,10,C,S)
=> all dz with ⇧Ca have ⇧clotting, strokes |
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what 5 things do endothelium release?
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• PreKallikrein
• Prostacyclin • Bradykininogen • t-PA • Makes Factors 5, 8, vWF |
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Prostacyclin
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vasodilation
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Bradykininogen
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⇨ BK (veno and vasodilator=> increase blood supply=> brings ATP)
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t-PA
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activates plasmin to break up clots
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PreKallikrein
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⇨ (HMW Kininogen) ⇨ Kallikrein
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how is a clot formed?
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1) Platelets plug up the hole loosely
2) Fibrin tightens it all up, sticks platelets to endothelium |
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what happens after clot is formed?
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>>Platelets release PDGF: stabilize fibroblasts
>>Endothelium releases EDGF and bradykinin: dilates vessels to bring 02 for energy |
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Lines of Zahn
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white clots that only occur in live people
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NormaL Platelets count:
<5OK ~> <20K ~> |
Platelets:
Normal-150-350K <5OK ~ steroids <20K ~ bleeding |
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Benard-Soulier
>>Inheritance >>pathogenesis >>presentation |
>>Autosomal Recessive
>>abnormal and big platelets (low GP1b) >>baby w/ bleeding from skin and mucosa, |
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Glanzmann's
>>Inheritance >>pathogenesis >>presentation |
>>Autosomal Recessive
>>abnormal platelets. (low GP2b3a) >>baby w/ bleeding from skin and mucosa |
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what disease have ⇧Platelets: (3)
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• Kawasaki
• Polycythemia Rubra Vera • Essential Thrombocythemia |
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Idiopathic Thrombocytopenic Purpura "ITP": antibody and child prognosis
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• Anti-platelet Ab
• Child petechiae (better prognosis in childhood) |
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Idiopathic Thrombocytopenic Purpura "ITP": Tx: (6)
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1) 60mg Prednisone
2) Immunoglobulin 3) Rituximab 4) Splenectomy (should leave Howell-Jolly bodies, if not ⇨ have an accessory spleen) 5)Azathioprine/Cyclophosphamide 6) Platelets (if <20k or bleeding) |
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Thrombotic Thrombocytopenic Purpura "TTP":
another name clue Tx |
• VWF Esterase Deficiency
• Young females w/seizures and big spleens • Tx: Plasmapheresis |
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DO NOT GIVE PLATELETS TO what diseases?
why? |
• TTP
• HUS • HIT (it just makes spleen eat more) |
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Factor 13 deficiency;
define tx |
umbilical stump bleeding
(1st time baby has to stabilize a clot) Tx: FFP |
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Protein C deficiency
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skin necrosis with Warfarin use
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Factor V Leiden
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Protein C can't break down Factor 5 => more clots
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Mild Bleeding (nosebleed) treatment
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DDAVP =Vasopressin= Desmopressin ⇨ Factor 5, 8, vWF
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Moderate Bleeding (heavy menstruation) treatment (3)
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Cryoprecipitate -Fibrinogen, Factor 8, vWF
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Severe Bleeding (shock) treatment
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FFP
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3 types of Von Willebrand's Disease, mode of inheritance and clue
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heavy menstruation
Type 1 (AD) Type 2 (AD) Type 3 (AR) |
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VWF Type 1
>>mode of inheritance >>pathogenesis |
(AD) Decreased VWF production
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Type 2 VWF
>>mode of inheritance >>pathogenesis >>test |
(AD)
Decreased VWF activity ( + ) Ristocetin aggregation test |
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Type 3 (AR)
what factor is decreased? |
No VWF, ⇩Factor 8
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Hemophilia A:
Mode of inheritance (who had it?) pathogenesis presentation |
XR =>uncle, grandpa had it
inactive Factor 8 (< 40% activity) Bleed into cavities (head, abdomen, pleural, pericardial, etc.) |
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Hemophilia B
mode of inheritance pathogenesis presentation |
mode of inheritance: XR
pathogenesis: Factor 9 deficiency "Christmas disease" presentation: Bleed into joints (knee, etc.) |
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Hemophilia C
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Factor 11 deficiency
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Chronic DIC
sign what is it due to? |
migratory thrombophlebitis
(due to lung, prostate, pancreatic, stomach CA) |
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what do thrombolytics do?
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plasminogen ⇨ plasmin ⇨ degrades fibrin ⇨ busts up clot
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t-PA :class and tx
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-thrombolytics
tx acute MI, strokes (<3 hrs) |
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Streptokinase: class SE
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thrombolytic that also inhibits fibrinogen=> more bleeding complications
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Urokinase: class and usage
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thrombolytic and used for open clotted fistulas
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antidote of thrombolytics
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Reverse w/ Aminocaproic Acid "Amicar"
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Alteplase
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another form of t-PA
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Platelet Haptens: (3)
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• asa
• Heparin • Quinidine |
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Thrombolytic Contraindications: (6)
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• Sytolic BP >180
• CPR >10 min • Recent sugery within 2wk • A Fib/MS/Pericarditis • Brain tumor/Head bleed history • Pregnancy |
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Platelet Inhibitors side effects
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bleeding from skin, mucosa
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COX Inhibitor
>>example >>MOA >>SE >>Contraindications |
>>asa
>>irreversibly inhibits COX >>cinchonism >>don't give if gout, asthma, hyperthyroid |
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name 2 Thrombin Blockers:
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• Argatroban
• Lepirudin |
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Argatroban
MOA when is it used how is it metabolized? |
blocks thrombin, use with HIT, liver metabolism
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Lepirudin
MOA when is it used how is it metabolized? |
blocks thrombin, use with HIT, kidney metabolism
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plasma vs serum
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Plasma: no RBC
Serum: no RBC or fibrinogen |
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PDE Inhibitors: (2)
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• Cilostazol
• Pentoxiphylline |
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PDE Inhibitors that dilates arteries
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Cilostazol
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GP2b3a Inhibitors:
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• Abciximab
• Eptifibatide "Integrilin" • Tirofiban |
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which GP2b3a Inhibitors makes Ab against GP2b3a =>rapid HIT (hours)?
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• Abciximab-
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Clopidogrel "Plavix": MOA and usage
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inhibits ADP, ⇩stroke in high-risk pts (w/ asa)
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Ticlopidine
class MOA SE (2) |
inhibits ADP needed for platelet fxn => agranulocytosis/seizures
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Dipyridamole: MOA and usage
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blocks ADP receptors
used in cardiac stress test (dilates vessels) |
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name all ADP Inhibitors:
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• Clopidogrel "Plavix"
• Ticlopidine • Dipyridamole |
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Heparin Induced Thrombocytopenia (HIT): 2 types
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HIT-1
HIT -2 |
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HIT2 definition and tx
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4-7 days ⇨ use Argatroban (liver metabolism) /Lepirudin (kidney metabolism)
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HIT-1 management
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immediate ⇨ don't stop heparin
UW: stop all heparin and replace with danaproid or lepeuridin or argatroban |
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Normal Labs:
Hb: Hct: pO2: |
Normal Labs:
Hb: 15 Hct: 3xHb pO2: 60-90 |
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define Erythropoiesis
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make new RBC
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what organ makes new RBC during < 1mo?
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yolk sac
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what organ does erythropoiesis at 1-2 months?
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Liver
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what organ does erythropoiesis at 2-4 month?
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Spleen/Lymph
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what organ does erythropoiesis at > 4mo?
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Bone Marrow
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what organ does erythropoiesis at 1y/o if damage primary organ? presentation
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long bones, your spleen can make RBC =>splenomegaly
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Hemoglobin HbA
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α2β₂ ⇦ adults
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HbA₂
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α₂δ₂ ⇦ minor component in adults
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HbF
when does it go away affinity for O2 |
α₂γ₂ ⇦ fetal, gone by 6 months, high affinity for O₂
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describe the heme synthesis:
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SuccinylCoA + Gly ⇨ ( δ-ALA synthase and ferrochelotase) ⇨ Heme
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what factors makes the Hb Curve shift to the right
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Shift to the Right: loss of O₂
''All CADETs face right" • ⇧ C02 • ⇧ Acid/ Altitude (⇧H+ =⇩pH) • ⇧ 2,3-DPG • ⇧ Exercise • ⇧Temp Note: pH is usually the answer, 'cuz that is what students mess up on |
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what factors makes the Hb curve Shift to the Left:
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• Mb
• MetHb • HbF (HbF holds on to O₂ HbF holds on to pO₂=40) • CO |
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what happens during exercise:
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• Blood flies through lungs (must sit still .075s to become fully saturated) ⇨ anaerobic
• ⇧lactic acid ⇨ muscle pain • The second wind => p02:60 ⇨ 40 (using Mb now) • Breathing hard after race = > repaying ATP to the body |
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Chronic Hypoxia:
mitochondria in the muscles what is the effect? |
More mitochondria in muscles
More EPO ⇨ ⇧Hct |
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when is a child normocytic until?
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normocytic until 2 month
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what is an acute Anemia?
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< 1wk
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what is an subacute Anemia?
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1-3 wk
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what is an chronic Anemia?
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>3 wk
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what are the microcytic anemias?
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Microcytic Hypochromic => Low Hb synthesis "FAST Lead"
Fe deficiency Anemia of Chronic Disease Pb poisioning Sideroblastic anemia Thalassemias |
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what are the causes of Fe deficiency? (6)
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Fe deficiency (menses, GI bleed, hookworms
colon CA, bad diet, <6 mo-no switch to HbA) |
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Iron deficiency presentation and labs
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Angular cheilosis (lip cracks), Koilonychia (spoon nails), Pica (eat ice, clay)
• Earliest sign: ⇧RDW • Low Ferittin (Fe storer) from GI mucosa • High TIBC (transferrin absorption) to get more Fe • Low Gastroferrin absorption in stomach • Low Lactoferrin in breast milk • High retic count (peaks on day 7) |
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treatment for iron deficiency
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Tx: Fe (Iron replacement: weight x Hb deficit)
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Ferritin
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Fe storer
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Transferrin
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Fe limo
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etiology of anemia of Chronic Disease:
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bone marrow shuts down; not replaced
• Plasma proteins kill off RBC • High Ferritin "Fe storer" (not being used=> piles up) • Low TIBC "Transferrin carrying capacity" (liver can't make transferrin) |
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during anemia of chronic disease, Plasma proteins kill off RBC? what is the tx for this?
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Tx: Epo
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EDTA
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X2+ binder:
Ca, Fe, Cu, Mg, Pb, Zn |
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lead poisoning presentation
who is high risk? symptoms (3) signs child's xray |
Kids that ate paint chips, pottery artists, firing range workers, battery workers
• Hypospermia, miscarriages, foot/wrist drop Bruton's lines =blue gumline • Child x-ray: lead lines in epiphyseal plates |
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lead poisoning labs (3)
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>>Basophilic stippling
>>Low ALA dehydrase and ferochelatase => can't make heme >>"Free erthrocyte protoporphyrins" =porphyrin rings that you can't add Fe to |
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test for lead poisoning
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Test: Ca-EDTA challenge=> lots of Pb excretion in urine
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what are 3 tx for lead poisoning?
function of each which one causes anaphylaxis which one is PO |
• Penicillamine - pulls X₂⁺ out of plasma => anaphylaxis
• Dimercaprol "BAL" - pulls Pb out of bone marrow • Succimer - binds Pb, oral agent |
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when do you hospitalize for lead poisoning?
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Hospitalize (> 30μg/ dL)
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when is EDTA given in lead poisoning?
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if Pb >45 μg/dL
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Enzymes that Need Pb:
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1) ALA dehydrase
2) Ferrochelatase |
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Sideroblastic anemia: etiology and cofactor
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low δ-ALA synthase <= Vit B6 cofactor (Ex: INH)
• Blood transfusions => Fe ppt => Sideroblasts, Pappenheimer bodies |
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what are the thalassemias: and describe the cells
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normal RDW (mostly small cells)
α-thalassemia β-thalassemia |
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α-thalassemia: chromosome
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Chr #16 deletion
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β-thalassemia
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Chr #11 point mutation
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Spherocytosis (AD)
type of anemia etiology pathogenesis |
Microcytic hyperchromic anemia. etiology is defective spherin
• Spherical RBC get stuck in spleen • RBC have no central area of pallor |
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test and tx for spherocytosis
what is a positive tests function of the tx |
Test: Osmotic fragility w/ hypotonic saline=> cells burst b/c they don't have spherin to protect
• Tx: Folate (to produce erythropoiesis) |
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Ferritin
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stores iron
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Transferrin
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transports iron
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TIBC
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transferrin absorption
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Fe Deficiency: Fe, TIBC, retics levels
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⇩Fe and ⇧TIBC levels with High retics
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Anemia of Chronic Disease: Fe, TIBC levels
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⇧Fe, ⇩TIBC levels. Just sittin' around . .. bone marrow shut down
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Pb Poisoning: Fe, TIBC.
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⇧Fe, nl TIBC
Don't need to bring in any more iron |
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Sideroblastic Anemia: Fe, TIBC.
what bodies does it form? |
⇧Fe, ⇧TIBC. Fe precipitates to form Pappenheimer bodies
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Hemochromatosis: labs Fe, TIBC, Ferritin and transferrin levels
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⇧Fe ⇧TIBC ⇧Ferritin >l000 ng/mL, ⇧Transferrin >50%
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what is the shape of RBC's
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biconcave shape
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what is a reticulocyte?
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Baby RBC
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normal reticulocyte?
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<l%
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what does it mean when there is a high reticulocyte?
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RBC being destroyed peripherally (bone marrow still functioning) ⇨ hemolytic anemia
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what does low reticulocytes mean?
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bone marrow not working
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RBC life span
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120 days
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Platelet life span
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7 days
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PMN life span
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1 day
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penia
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low
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cytosis
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high
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cythemia
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high
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RBC Measurements: big cells: MCH and MCHC
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normal MCH, low MCHC
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RBC count
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how many RBCs there are
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Reticulocyte count: low =>
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decreased production,
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reticulocyte is high =>
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RBC desruction
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Hb concentration
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how much Hb you have
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RDW
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RBC distribution width => anisocytosis (cell size variation)
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Hematocrit: how to find out and and how to calculate
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Add EDTA and centrifuge => RBC vol/Total vol
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MCV: what it stands for? ratio between what two values and what does it tell you?
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mean cell volume => hematocrit/ RBC count => micro/ macrocytic
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MCH: what it stands for and what does it tell you?
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mean cell Hb => hypo/ hyperchromic
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MCHC
what it stands for units what does it tell you? |
mean cell Hb conc = #g Hb/dL RBC => hypo/hyperchromic
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Acute Intermittent Porphyria etiology
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⇧Porphyrin production, urine δ-ALA, ⇧urine porphobilinogen
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Acute Intermittent Porphyria presentation
symptoms can be triggered by what factors? |
Abdominal pain, neuropathy, red urine (hemolytic anemia)
Can be set off by stress (menses, Drugs: Barbs, Sulfas) |
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Acute Intermittent Porphyria Tx: (4 steps and why)
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1. Fluids -wash away porphyrin ring
2. Sugar - break down bilirubin 3. Opiates - stop pain (use Meperidine for abdominal pain) 4. Hematin - inhibits δ-ALA synthase |
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Porphyria Cutanea Tarda: describe
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: Sunlight=> bullae w/ porphyrin deposits
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Porphyria Cutanea Tarda: associated disease
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Assoc w/ Hep C
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Porphyria Cutanea Tarda: tx
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Tx: Plasmapheresis
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Porphyria Cutanea Tarda: wood's lamp
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Wood's lamp= orange-pink
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Porphyria Cutanea Tarda: urine
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⇧ urine porphyrine
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Erythrocytic Protoporphyria:
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Porphyria cutanea tarda in a baby
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what happens when HbS polymerizes
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sickling in kidney vasa recta
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Sickle Cell Disease
mode of inheritance type of hemoglobin etiology |
(AR) Homozygous
HbS (βglu6⇨val) |
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Sickle Cell Disease presentation (3)
when does painful fingers/toes appear xray what is pain referred to the knee with sickle cell disease? |
>>Dactylitis (painful fingers/toes) at 6mo, short fingers
>>"Crew haircut" on x-ray >>Vasa-occlusion: spleen infarction, avascular necrosis of femur (pain referred to knee) |
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Sickle Cell Disease tx, prevention (2) and tx for sickle cell crisis
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o Hydroxyurea (⇧HbF)
o Folate (prevent aplastic crisis) o Pneumococcal vaccine o Sickle cell crisis Tx: O₂, PRBC |
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sickle cell disease suceptible infections
what does it lead to? |
⇧Salmonella/Parvo B-19 infections ⇨ aplastic crisis
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Aplastic Crisis
retic level pathogenesis |
RBCs stop being made (no retics)
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Splenic Sequestration Crisis
retic level location |
RBCs trapped in spleen (high retics)
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Thick Stomach Rugal Folds: Dx
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Menetrier's
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Absent Stomach Rugal Folds: Dx
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Pernicious Anemia
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Sickle cell anemia:
complication of sickle cells what pathogens succeptible to? what can these lead to? tx |
sickle in kidney vasa recta
• Salmonella, ParvoB-19 infxns => aplastic anemia • Tx: O₂, hydroxyurea, pneumococcal vaccine |
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Sickle Cell Trait
common presentation what profession they cannot be in and why? type of hemoglobin |
>>painless hematuria, sickle with extreme hypoxia (can't be a pilot, fireman)
>>Heterozygous HbS |
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HbC Disease
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(βglu6 ~> Lys), still charged = > no sickling
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PRBC: 1 unit (500mL)
only transfuse if sx ... |
• ⇧ Hb by 1-2g/ dL
• ⇧ Fe by 3-4g/dL |
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α-Thalassemias: has how many genes (Hb subunit)
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4 genes
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β Thalassemias: how many genes (Hb subunit)
|
2 genes
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α- thalassemia: ch deletion and ethnicity
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(Chr.16 deletion) - AA, Asians
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α- thalassemia: 1 deletion
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normal
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α- thalassemia: 2 deletions "trait"
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microcytic anemia
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α- thalassemia: 3 deletions
kind of anemia type of hemoglobin ppt with what compound |
hemolytic anemia, Hb H = β4 (ppt w / brilliant cresyl blue)
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α- thalassemia: 4 deletions
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hydrops fetalis (stillborn baby), Hb Bart = γ4
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β-thalassemia:
chromosomal deletion more common in what ethnicity |
(Chr.11 point mutation) - Mediterraneans
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β-thalassemia: 1 deletion "β minor"
what are the hemoglobins? |
more HbA₂ and HbF
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β-thalassemia: 2 deletions
name hemoglobin present presentation |
"trait/intermedia/major" =>only HbA2 and HbF =>hypoxia at 6 mo
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Cooley's Anemia
where is this seen describe the pathogenesis |
see w/ β-thalassemia major
(no HbA =>excess RBC production) |
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Baby making blood from everywhere ~> frontal bossing, hepatosplenomegaly, long
extremities |
Cooley's Anemia
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treatment for cooley's anemia
and its complication tx |
• Tx: Total body transfusion q60-90 days~> hemochromatosis (Tx: Defuroxamine)
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Anemia: criterias, effects
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(Hb <11 for everybody), less Hb => less 02 carrying capacity
<9 => moderate <7 =>severe |
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effects of anemia on CO and PP, skin, cardiac cells and neurons
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⇩02 transport ⇨ dilate arterioles ⇨ ⇩blood return to heart ⇨ ⇧CO, ⇧PP
• Skin atrophy • Fatty cardiac mvocytes • Neuron degeneration |
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Thrombosis Risk Factors:
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"Virchow' s triad"
1) Turbulent blood flow "slow" 2) Hypercoaguable "stick'" 3) Vessel wall damage "escapes" |
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Hypoxia Acute presentation
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SOB
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Hypoxia Chronic
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Clubbing of fingers/toes
(furthest from blood supply) |
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Cyanosis
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5g Hb fully desaturated at this moment
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who will be more cyanotic, anemic or polycythemic patients
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An anemic person will rarely be cyanotic b / c 5g will be a bigger percentage of their Hb
• Easier for polycythemic pts to become cyanotic b / c they have more grams of Hb available |
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Hemolysis Intravascular:
where is the RBC destroyed? haptaglobin levels ex |
RBC destroyed in blood v v. ~> low haptoglobin (binds free floating Hb)
• Ex: Vasculitis |
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Hemolysis Extravascular:
location presentation ex |
RBC destroyed in spleen (problem w/ RBC membrane)=> splenomegaly
• Ex: Hemolytic anemias |
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Megaloblastic anemia
pathogenesis pathopneumonic |
gets bigger, can't divide ⇨ hypersegmented neutrophils
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give 2 causes of Vit B12 deficiency
how where is B12 absorbed |
tapeworms, vegans
R-Vit B 12 ⇨ binds IF (in ileum). need pancreatic enzmes to cleave R off. |
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Vit B12 deficiency: presentation
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(⇩pain and temp,+ Romberg test due to neuro sx)
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Type A Gastritis:
another name antibody |
atrophic gastritis
• Anti-parietal cell Ab |
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Pernicious anemia:
surgery cancer association presentation of stomach |
s/p terminal ileumectomy, ⇧gastric CA, absent stomach ruggae
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Pernicious anemia: labs
antibodies test enzymes |
Anti-IF Ab, (+)Schilling test, ⇧MMA, ⇧Homocysteine
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Pernicious anemia: enzymes
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MMCoA mutase- recycles odd carbons
• Homocysteine Me-Transferase - makes THF (need for nucleotide synthesis) |
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Schilling Test: (+) IF reabsorption ⇨Dx
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label Vit B12
pernicious anemia |
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Schilling Test (+) Antibiotic reabsorption ⇨ Dx
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bacterial overgrowth
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Folate deficiency:
presentation causes: drugs and food |
due to eating old, overcooked food=> glossitis (beefy red tongue)
• drugs: Phenytoin, Phenobarbital, Bactrim |
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Alcohol:
disease in a new born baby presentation of baby |
Fetal EtOH syndrome:
smooth philtrum, stuff doesn't grow, mental retardation |
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Smooth Philthrum
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Fetal EtOH
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Long Philthrum
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wililliam's
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Anticonvulsants that can cause megaloblastic anemia (4)
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"P CaVE"
• Phenytoin • Carbamazepine • Valproic acid • Ethosuximide |
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RBC Haptens:
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"PAD PACS"
• Penicillamine • α-MeDopa • Dapsone • PTU • Antimalarials • Cephalosporins • Sulfa drugs |
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what can cause megaloblastic anemias
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vit b12 def
folate deficiency anticonvulsuants (carbamazepine, phenytoin, valproic acid and ethosuximide) alcohol |
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what are the hemolytic anemias?
macro/micro 2 types |
the macrocytosis anemias: extra and intravascular anemias
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3 intravascular hemolytic anemias:
what is the antibody that is used? |
IgM
G-6-PD Deficiency Cold Autoimmune Paroxysmal Nocturnal Hemoglobinuria |
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2 Extravascular hemolytic anemias and what antibody is used?
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IgG
Warm Autoimmune Paroxysmal Cold Autoimmune |
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Sausage digits
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Pseudo hypoPTH
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6 fingers
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Trisomy 13
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2-jointed thumbs
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Diamond-Blackfan anemia
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Painful fingers
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Sickle cell anemia
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G-6-PD Deficiency
mode of inheritance presentation, labs MOA of G6PD |
(XR) jaundice, dark urine, sudden drop Hb (> 3g/ dL),
unconjugated hyperbilirubin • Mechanism: HMP shunt ⇨ G-6-PD ⇨ GSH (protects RBC against oxidation) |
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drugs that can cause G-6-PD Deficiency
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Drugs:
o Sulfa drugs: Dapsone o Naphthalene moth balls o Fava beans |
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G-6-PD Deficiency CI and tx
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Tx: IVF to protect kidneys (no asa)
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Cold Autoimmune
pathogenesis (3) give 2 examples |
RBC agglutination, fixes complement, active in distal body parts
• Post-mycoplasma infection • Mononucleosis infection |
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Paroxysmal Nocturnal Hemoglobinuria: etiology and presentation (3)
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>>The only hemolytic anemia caused by an acquired cell-membrane defect
>>Hemolytic anemia, thrombosis, red urine |
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Paroxysmal Nocturnal Hemoglobinuria: test
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(+)Ham's acid hemolysis, Sugar-water test
• Flow cytometry: CD55/CD59 |
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Warm Autoimmune: antibody and when is it active
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anti-Rh Ab, active at body temp
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Warm Autoimmune: drugs
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drugs: The RBC Haptens (PAD PACS)
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Warm Autoimmune: tx
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Tx: Steroids, Splenectomy
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Paroxysmal Cold Autoimmune: etiology, ab and presentation
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>>fixes complement
>>Donath-Landsteiner Ab >>Massive bleeding after cold exposure |
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Production Anemias:
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Diamond-Blackfan:
Aplastic Anemia "pancytopenia" |
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Diamond-Blackfan
pathogenesis what enzyme is increased presentation |
kid is born without RBCs (high adenosine deaminase), 2-jointed thumbs
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Aplastic Anemia "pancytopenia":
Labs virus autoimmune drugs |
⇩RBC/ ⇩WBC/ ⇩Platelets
>>T-cell induced apoptosis of progenitor cells (autoimmmne ~> thymoma) >>Virus: ParvoB-19, HepC (transfusions), HepE (pregnant women), EBV >>Drugs: ABCV" o AZT o Benzene o Chloramphenicol o Vinblastine |
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Aplastic Anemia "pancytopenia": tx
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Tx: Immnnosuppresion or Bone marrow transplant
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Basophilic stippling:
type of cell stain disease what are the stippling? |
Lots of immature cells => ⇧mRNA, stain blue (Pb poisoning)
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Bite cell
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Hemolysis
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Doehle body:
define give 3 causes (in order) |
PMN leukocytosis
#1 cause: Infection #2 cause: Corticosteroids #3 cause: Tumor |
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Burr cell
another name 3 causes |
Echinocyte
Pyruvate kinase deficiency, Liver dz, Post-splenectomy |
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Cabot's ring body
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Vit B12 deficiency, Pb poisoning
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Drepanocyte
another name where is it found |
Sickle cell
Sickle cell anemia |
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Helmet cell
define give 3 causes |
fragmented RBC (Hemolysis: DIC, HUS, TTP)
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Heinz body
disease how is it made? |
Hb denatures and sticks to cell membranes (G-6PD deficiency)
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Howell-Jolly body:
describe etiology (3 causes) |
Spleen or bone marrow should have removed nuclei fragments
#1 : Spleen trauma #2: Hemolytic anemia #3: Cancer |
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Pappenheimer bodies
define where is it found? |
Fe ppt inside cell
(Sideroblastic anemia) |
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Pencil cell
another name deficiency |
Cigar cell: Fe deficiency anemia
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Rouleaux formation:
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Multiple myeloma
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Schistocyte
define where is it found? |
Broken RBCs (DIC, artificial heart valves)
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Sideroblast
define where is it found? |
MP pregnant with iron
(Genetic or Multiple transfusions) |
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Spherocytes
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(AD): Old RBCs
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Spur cell
another name disease |
Acanthocyte: Lipid bilayer dz
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1) Stomatocyte:
2) Target cells |
1) EtOH, liver dz
2) less Hb (thallasemias) |
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Tear drop cell
another name define where is it found? |
Dacrocyte
RBCs squeezed out of marrow (Hemolytic anemia, Bone marrow cancer) |
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what clotting factor does Kallikrein activate?
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factor 11
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what clotting factor does clotting factors 8 and 10 activate?
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factor 10
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what clotting factor does clotting factor 5 activate?
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factor 2
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what does protein C and S inhibit?
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factors 8 and 5
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what does heparin (indirectly) and anti-thrombin III inhibit?
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factor 2
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what does warfarin inhibit?
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factors 2,7, 9,10 and protein c and s
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