Notes in ✧ Hemostasis

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Published	01/14/2024	Central diabetes insipidus is treated with a(n) {{c1::ADH}} analogue, such as {{c2::dDAVP (desmopressin)}}
Published	01/14/2024	Treatment for central diabetes insipidus includes hydration and {{c1::desmopressin}}, which is an ADH analog
Published	01/14/2024	In addition to central diabetes insipidus, desmopressin (DDAVP) may be used to treat {{c1::von Willebrand disease}}, which is associated with increase…
Published	01/14/2024	Desmopressin may be used to treat night {{c1::enuresis (bed wetting)}}
Published	01/14/2024	Bradykinin causes arteriolar {{c1::dilation}} and venous {{c1::constriction}}
Published	01/14/2024	Treatment of acute coronary syndromes (e.g. unstable angina, STEMI, NSTEMI) often includes antiplatelet therapy such as {{c1::aspirin}}
Published	01/14/2024	The most common cause of aortic stenosis is {{c1::degenerative calcification}} from "wear and tear"
Published	01/14/2024	Primary hemostasis is mediated by interactions between {{c1::platelets}} and the {{c2::vessel wall}}
Published	01/14/2024	Secondary hemostasis is mediated by the {{c1::coagulation cascade}}
Published	01/14/2024	The first step of primary hemostasis is {{c1::transient vasoconstriction}} of the damaged vessel; which is mediated by {{c2::reflex neural}} stimulati…
Published	01/14/2024	Following transient vasoconstriction (primary hemostasis), there is platelet {{c1::adhesion}} to the surface of the disrupted vessel
Published	01/14/2024	When a blood vessel is injured, {{c1::von Willebrand factor (vWF)}} binds exposed {{c2::subendothelial collagen}}
Published	01/14/2024	In order to adhere to the damaged endothelium, platelets bind {{c1::vWF}} using the {{c2::GPIb}} receptor
Published	01/14/2024	One source of von Willebrand factor (vWF) is from the {{c1::Weibel-Palade bodies}} of {{c2::endothelial cells}}
Published	01/14/2024	One source of von Willebrand factor (vWF) is from the {{c1::α}} granules of {{c2::platelets}}
Published	01/14/2024	Following platelet adhesion (primary hemostasis), there is platelet {{c1::degranulation::not aggregation}}
Published	01/14/2024	Binding of ADP to the P2Y12 receptor in primary hemostasis causes {{c1::shape}} change by upregulating intracellular {{c2::Ca2+}}, promoting effective…
Published	01/14/2024	Binding of ADP to the P2Y12 receptor promotes optimal exposure of the {{c1::GPIIb/IIIa}} receptor on platelets
Published	01/14/2024	Binding of ADP to the P2Y12 receptor leads to {{c2::decreased}} {{c1::cAMP}} formation which favors platelet activation
Published	01/14/2024	What ion is released from dense granules of platelets during degranulation? {{c1::Ca2+}}
Published	01/14/2024	Thromboxane A2 (TXA2) is synthesized by the platelet enzyme {{c1::cyclooxygenase-1 (COX-1)::specific}}
Published	01/14/2024	Thromboxane A2 promotes platelet {{c1::aggregation}}
Published	01/14/2024	Following upregulation of GpIIb/IIIa, platelets aggregate at the site of injury via crosslinking of GpIIb/IIIa receptors with {{c1::fibrinogen}} to ma…
Published	01/14/2024	Binding between GPIIb/IIIa and fibrinogen results in formation of a(n) {{c1::weak platelet plug}}
Published	01/14/2024	Disorders of primary hemostasis present with symptoms of mucosal and skin {{c1::bleeding}}
Published	01/14/2024	Disorders of primary hemostasis present with symptoms of mucosal bleeding, such as {{c1::epistaxis}} (most common overall symptom)
Published	01/14/2024	Quantitative disorders of primary hemostasis present with symptoms of skin bleeding, such as {{c1::petechiae}} (1-2 mm)
Published	01/14/2024	Petechiae are a sign of thrombocytopenia and are not usually seen with {{c1::qualitative}} platelet disorders
Published	01/14/2024	Bleeding time is normally between {{c1::2}} and {{c1::7}} minutes
Published	01/14/2024	{{c2::Bleeding time}} is {{c1::prolonged}} in all platelet disorders (both quantitative and qualitative)
Published	01/14/2024	{{c1::Immune thrombocytopenic purpura (ITP)}} is due to autoimmune production of Ig{{c2::G}} against {{c3::GPIIb/IIIa}}
Published	01/14/2024	The autoantibodies in ITP are produced by plasma cells in the {{c1::spleen}}
Published	01/14/2024	The antibody-bound platelets in ITP are consumed by {{c1::splenic macrophages}}, resulting in thrombocytopenia
Published	01/14/2024	What demographic is associated with the chronic form of immune thrombocytopenic purpura? {{c1::Women of childbearing age}}
Published	01/14/2024	Immune thrombocytopenic purpura presents with {{c1::increased}} bleeding time / PFA
Published	01/14/2024	The treatment for refractory cases of ITP is {{c1::splenectomy}}
Published	01/14/2024	{{c1::Microangiopathic hemolytic}} anemia occurs when RBCs are "sheared" as they cross {{c2::microthrombi}}
Published	01/14/2024	Microangiopathic hemolytic anemia is often associated with formation of platelet {{c1::microthrombi}} in small vessels
Published	01/14/2024	Microangiopathic hemolytic anemia is seen in {{c1::TTP}}, {{c2::HUS}}, and {{c3::HELLP}} syndrome
Published	01/14/2024	What type of red blood cell is associated with microangiopathic hemolytic anemia? {{c1::Schistocytes ("helmet cells")}}
Published	01/14/2024	{{c2::Thrombotic thrombocytopenic purpura (TTP)}} is due to inhibition or deficiency of the {{c1::ADAMTS13 (vWF metalloprotease)}} enzyme
Published	01/14/2024	In TTP, large, uncleaved vWF multimers lead to increased platelet {{c1::adhesion}} with consequent {{c2::microthrombi}} formation
Published	01/14/2024	Decreased ADAMTS13 (e.g. TTP) is usually due to an acquired {{c1::autoantibody}}
Published	01/14/2024	The pentad of classical symptoms seen in {{c6::thrombotic thrombocytopenic purpura (TTP)}} may be remembered using the mnemonic FAT RN: F: {{c1::Fever…
Published	01/14/2024	What is the treatment (3) for thrombotic thrombocytopenic purpura (TTP)? {{c1::plasmapheresis}}, {{c2::corticosteroids}}, {{c3::rituximab}}
Published	01/14/2024	{{c1::Hemolytic uremic syndrome (HUS)}} is characterized by thrombocytopenia, microangiopathic hemolytic anemia, and {{c2::acute renal failure}}
Published	01/14/2024	{{c2::Hemolytic uremic}} syndrome is classically seen in {{c3::children}} with {{c1::E. coli O157:H7}} dysentery, which results from exposure to …
Published	01/14/2024	TTP and HUS present with {{c1::increased}} bleeding time
Published	01/14/2024	TTP and HUS present with {{c1::decreased}} platelet count
Published	01/14/2024	TTP and HUS typically present with {{c1::normal}} PT and {{c1::normal}} PTT
Published	01/14/2024	The initial treatment for hemolytic uremic syndrome (HUS) is {{c1::plasmapheresis}}
Published	01/14/2024	{{c2::Bernard-Soulier}} syndrome is a qualitative platelet disorder due to a genetic {{c1::GPIb}} deficiency
Published	01/14/2024	{{c2::Bernard-Soulier}} syndrome is characterized by {{c1::enlarged platelets}} on blood smear
Published	01/14/2024	In Bernard-Soulier syndrome there is a defect in platelet {{c1::adhesion}}
Published	01/14/2024	{{c2::Glanzmann thrombasthenia}} is a qualitative platelet disorder due to a genetic {{c1::GPIIb/IIIa}} deficiency
Published	01/14/2024	In Glanzmann thrombasthenia there is a defect in platelet {{c1::aggregation}}
Published	01/14/2024	Glanzmann thrombasthenia is characterized by no {{c1::platelet}} clumping on blood smear
Published	01/14/2024	Bernard-Soulier syndrome presents with {{c1::increased}} bleeding time
Published	01/14/2024	Bernard-Soulier syndrome presents with {{c1::normal}} or {{c1::decreased}} platelet count
Published	01/14/2024	Glanzmann thrombasthenia presents with {{c1::increased}} bleeding time
Published	01/14/2024	Glanzmann thrombasthenia presents with {{c1::normal}} platelet count
Published	01/14/2024	Aspirin irreversibly inactivates the enzyme {{c1::cyclooxygenase}}, thus decreasing synthesis of {{c2::TXA2}} and impairing platelet {{c3::aggregation…
Published	01/14/2024	The coagulation cascade generates {{c1::thrombin (factor IIa)}}, which converts fibrinogen in the platelet plug to {{c2::fibrin (factor Ia)}} *BnB exp…
Published	01/14/2024	After fibrin is formed from fibrinogen, it is {{c1::cross-linked}} by factor {{c2::XIII}} yielding a stable platelet-fibrin thrombus
Published	01/14/2024	Factors of the coagulation cascade are produced by the {{c1::liver}} in an inactive state
Published	01/14/2024	Activation of the coagulation cascade requires the {{c1::phospholipid}} surface of platelets
Published	01/14/2024	Activation of the coagulation cascade requires {{c1::Ca2+}} ions derived from platelet {{c2::dense}} granules
Published	01/14/2024	Disorders of secondary hemostasis typically present with {{c1::deep tissue::location}} bleeding
Published	01/14/2024	{{c1::Prothrombin time (PT)}} measures the {{c2::extrinsic}} and common pathways of the coagulation cascade
Published	01/14/2024	{{c1::Partial thromboplastin time (PTT)}} measures the {{c2::intrinsic}} and common pathways of the coagulation cascade
Published	01/14/2024	International normalized ratio (INR) is calculated from {{c1::PT::PT or PTT}}
Published	01/14/2024	Which coagulation factor(s) are part of the extrinsic coagulation cascade? {{c1::Factor VII}}
Published	01/14/2024	Which coagulation factor(s) are part of the intrinsic coagulation cascade? {{c1::Factor 8, 9, 11, 12}}
Published	01/14/2024	Which coagulation factor(s) are part of the common coagulation cascade? {{c1::Factor 10, 5, 2 (thrombin), 1 (fibrinogen)}}
Published	01/14/2024	Factor XI of the coagulation cascade is activated by factor {{c1::XIIa}}
Published	01/14/2024	Factor IX of the coagulation cascade is activated by factor {{c1::XIa}}
Published	01/14/2024	Factor X of the coagulation cascade may be activated by factor {{c1::VIIa}} (extrinsic pathway)
Published	01/14/2024	Factor V of the coagulation cascade is activated by factor {{c1::IIa}}
Published	01/14/2024	Factor II (prothrombin) is activated to thrombin by factor {{c1::Xa}}
Published	01/14/2024	{{c1::Tissue thromboplastin}} activates factor {{c2::VII}}, which initiates the extrinsic pathway of the coagulation cascade
Published	01/14/2024	{{c1::Subendothelial collagen}} activates factor {{c2::XII}}, which initiates the intrinsic pathway of the coagulation cascade
Published	01/14/2024	Hemophilia {{c1::A}} is a coagulation disorder due to a genetic factor {{c2::VIII}} deficiency
Published	01/14/2024	What is the mode of inheritance of hemophilia A? {{c1::X-linked recessive}}
Published	01/14/2024	Hemophilia A can arise from a(n) {{c1::new (de novo)}} mutation without any family history (20%)
Published	01/14/2024	Which coagulation disorder presents with recurrent hemarthroses, spontaneous / easy bruising, and bleeding after surgery? {{c1::Hemophilia (A, B, C)}}
Published	01/14/2024	Hemophilia {{c1::B (Christmas disease)}} is a coagulation disorder due to a genetic factor {{c2::IX}} deficiency
Published	01/14/2024	What is the mode of inheritance of hemophilia B? {{c1::X-linked recessive}}
Published	01/14/2024	Hemophilia {{c1::C}} is a coagulation disorder due to a genetic factor {{c2::XI}} deficiency
Published	01/14/2024	What is the mode of inheritance of hemophilia C? {{c1::Autosomal recessive}}
Published	01/14/2024	Treatment of hemophilia A involves {{c1::desmopressin}} plus recombinant {{c2::factor VIII}}
Published	01/14/2024	Hemophilia (A, B, C) presents with {{c1::normal}} bleeding time
Published	01/14/2024	Hemophilia (A, B, C) presents with {{c1::normal}} platelet count
Published	01/14/2024	Hemophilia (A, B, C) presents with {{c1::normal}} PT and {{c1::increased}} PTT
Published	01/14/2024	A coagulation factor inhibitor is a(n) {{c1::acquired antibody}} against a coagulation factor, resulting in impaired factor function
Published	01/14/2024	What is the most common coagulation factor inhibitor?{{c1::Anti-Factor VIII}}
Published	01/14/2024	In hemophilia A, mixing normal plasma with the patient's plasma (mixing study) {{c1::does::does/doesn't}} correct the PTT
Published	01/14/2024	With a factor VIII coagulation factor inhibitor, mixing normal plasma with a patient's plasma {{c1::doesn't::does/doesn't}} correct the PTT
Published	01/14/2024	{{c1::Von Willebrand disease}} is characterized by a genetic vWF deficiency
Published	01/14/2024	What is the most common inherited bleeding/coagulation disorder? {{c1::von Willebrand disease}}
Published	01/14/2024	What is the mode of inheritance of the most common subtype of von Willebrand disease? {{c1::Autosomal dominant}}
Published	01/14/2024	The most common subtype of von Willebrand disease presents with {{c1::decreased}} vWF levels
Published	01/14/2024	von Willebrand disease typically presents with mild {{c1::mucosal::locations}} and {{c1::skin}} bleeding
Published	01/14/2024	Low vWF in von Willebrand disease impairs platelet {{c1::adhesion}}
Published	01/14/2024	von Willebrand disease presents with {{c1::increased}} bleeding time
Published	01/14/2024	von Willebrand disease presents with {{c1::normal}} platelet count
Published	01/14/2024	von Willebrand disease presents with {{c1::normal}} PT and {{c1::normal}} or {{c1::increased}} PTT
Published	01/14/2024	Why may PTT be elevated in von Willebrand disease? {{c1::Decreased factor VIII half-life (vWF normally stabilizes factor VIII)}}
Published	01/14/2024	von Willebrand disease is associated with an abnormal {{c1::Ristocetin}} assay
Published	01/14/2024	Ristocetin induces platelet aggregation by causing {{c1::vWF}} to bind platelet GPIb
Published	01/14/2024	What is the treatment for von Willebrand disease?{{c1::Desmopressin}}
Published	01/14/2024	Desmopressin increases release of {{c1::vWF}} from {{c2::Weibel-Palade bodies}}
Published	01/14/2024	Vitamin K is necessary for {{c1::gamma carboxylation}} of factors II, VII, IX, X, and proteins C and S
Published	01/14/2024	Which coagulation factors have decreased activity due to vitamin K deficiency? {{c1::2, 7, 9, 10::4}}
Published	01/14/2024	What proteins have decreased activity due to vitamin K deficiency? {{c1::Protein C and protein S::2}}
Published	01/14/2024	Vitamin K deficiency may occur in {{c1::newborns}} due to lack of {{c2::colonic bacteria}} that normally synthesize vitamin K
Published	01/14/2024	Vitamin K deficiency may occur due to long-term {{c1::antibiotic}} therapy, which disrupts the gut flora
Published	01/14/2024	Vitamin K deficiency may occur due to {{c1::fat}} malabsorption, which leads to deficiency of fat-soluble vitamins
Published	01/14/2024	Vitamin K deficiency presents with {{c1::normal}} bleeding time
Published	01/14/2024	Vitamin K deficiency presents with {{c1::increased}} PT and {{c1::increased (in severe cases)}} PTT
Published	01/14/2024	Abnormal secondary hemostasis may occur due to {{c1::liver}} failure, which causes decreased production of coagulation factors and decreased acti…
Published	01/14/2024	Abnormal secondary hemostasis may occur due to {{c1::liver}} failure, which causes decreased activation of vitamin K
Published	01/14/2024	Abnormal secondary hemostasis may occur due to {{c1::large-volume transfusion}}, which dilutes coagulation factors, resulting in a relative deficiency
Published	01/14/2024	Alpha granules of platelets contain {{c1::vWF}} and fibrinogen
Published	01/14/2024	Dense granules of platelets contain {{c1::Ca2+}} and {{c2::ADP}}
Published	01/14/2024	Heparin-induced thrombocytopenia is a disorder that results in platelet {{c1::activation}} secondary to heparin therapy
Published	01/14/2024	Heparin-induced thrombocytopenia occurs due to production of Ig{{c1::G}} antibodies against {{c2::heparin-platelet factor IV}} complexes
Published	01/14/2024	The antibody-heparin-PF4 complex may activate {{c1::platelets}}, leading to thrombosis and thrombocytopenia
Published	01/14/2024	{{c1::Disseminated intravascular coagulation (DIC)}} occurs due to pathologic activation of the coagulation cascade
Published	01/14/2024	Disseminated intravascular coagulation (DIC) is characterized by widespread {{c1::microthrombi}} formation, resulting in ischemia and infarction
Published	01/14/2024	In disseminated intravascular coagulation, consumption of platelets and factors results in {{c1::bleeding}}
Published	01/14/2024	{{c8::Disseminated Intravascular Coagulation (DIC)}} is almost always secondary to another disease, which may be remembered with "STOP Making New…
Published	01/14/2024	Disseminated intravascular coagulation may occur secondary to obstetric complications due to activation of the coagulation cascade by {{c1::tissu…
Published	01/14/2024	Disseminated intravascular coagulation may occur secondary to sepsis, especially gram {{c1::negative}} bacteria
Published	01/14/2024	Disseminated intravascular coagulation may occur secondary to malignancy, such as {{c1::adenocarcinoma}}, due to activation of the coagulation ca…
Published	01/14/2024	Disseminated intravascular coagulation may occur secondary to malignancy, such as {{c1::acute promyelocytic leukemia}}, due to activation of the …
Published	01/14/2024	DIC typically presents with {{c1::increased}} bleeding time
Published	01/14/2024	What type of red blood cell is associated with disseminated intravascular coagulation? {{c1::Schistocytes (due to microangiopathic hemolytic anemia)}}
Published	01/14/2024	D-dimers are derived from splitting of {{c1::cross-linked fibrin}}
Published	01/14/2024	Are D-dimers generated from the splitting of fibrinogen? {{c1::No}}
Published	01/14/2024	Treatment of DIC includes transfusion of blood products and {{c1::cryoprecipitate}} as needed
Published	01/14/2024	In the first step of fibrinolysis, {{c1::plasminogen}} is converted to {{c2::plasmin}} via {{c3::tissue plasminogen activator (tPA)}}
Published	01/14/2024	One role of plasmin is {{c1::cleavage}} of fibrin and serum fibrinogen
Published	01/14/2024	One role of plasmin is {{c1::destruction}} of coagulation factors
Published	01/14/2024	Plasmin is inactivated by {{c1::α2-antiplasmin}}, which is produced in the liver
Published	01/14/2024	Disorders of fibrinolysis are due to {{c1::plasmin}} overactivity, resulting in excessive cleavage of serum {{c2::fibrinogen}}
Published	01/14/2024	Over-activity of plasmin may occur due to activation by {{c2::urokinase}}, which is released following radical {{c1::prostatectomy}}
Published	01/14/2024	Over-activity of plasmin may occur due to reduced production of {{c1::α2-antiplasmin}} by the liver (e.g. cirrhosis)
Published	01/14/2024	Disorders of fibrinolysis present with increased {{c1::bleeding}} (resembles DIC)
Published	01/14/2024	Disorders of fibrinolysis typically present with {{c1::increased}} PT and {{c1::increased}} PTT
Published	01/14/2024	Disorders of fibrinolysis typically present with {{c1::normal}} platelet count
Published	01/14/2024	Disorders of fibrinolysis typically present with {{c1::increased}} bleeding time
Published	01/14/2024	Disorders of fibrinolysis typically present with {{c1::decreased}} fibrinogen
Published	01/14/2024	Disorders of fibrinolysis typically present with increased {{c1::fibrinogen}} split products
Published	01/14/2024	Do disorders of fibrinolysis present with elevated D-dimers? {{c1::No}}
Published	01/14/2024	Treatment for disorders of fibrinolysis is {{c1::aminocaproic acid}}, which blocks activation of {{c2::plasminogen}}
Published	01/14/2024	Factor X of the coagulation cascade may be activated by factor {{c1::IX}} with factor {{c1::VIII}} as a cofactor (intrinsic pathway)
Published	01/14/2024	The three major risk factors for thrombosis are {{c1::disruption in blood flow (stasis)}}, {{c2::hypercoagulability}}, and {{c3::endothelial cell dama…
Published	01/14/2024	Endothelial cells prevent thrombosis by producing {{c1::prostacyclin (PGI2)}} and {{c2::NO}}
Published	01/14/2024	{{c2::Prostacyclin (PGI2)}} and {{c3::NO}} from endothelial cells cause inhibition of platelet {{c1::aggregation}}
Published	01/14/2024	Endothelial cells prevent thrombosis by secreting {{c1::heparin-like}} molecules, which augment {{c2::antithrombin III (ATIII)}}
Published	01/14/2024	Antithrombin III {{c1::inactivates::activates or inactivates}} thrombin and coagulation factors
Published	01/14/2024	Endothelial cells prevent thrombosis by secreting {{c1::tissue plasminogen activator (tPA)}}, which converts plasminogen to plasmin
Published	01/14/2024	Endothelial cells prevent thrombosis by producing {{c3::thrombomodulin}}, which redirects {{c1::thrombin}} to activate {{c2::protein C}}
Published	01/14/2024	Which amino acid may cause endothelial cell damage when serum levels are elevated? {{c1::Homocysteine}}
Published	01/14/2024	Vitamin B12 and folate deficiency result in mildly elevated {{c1::homocysteine}} levels, increasing risk for thrombosis
Published	01/14/2024	Which vitamin deficiencies are associated with increased risk for thrombosis? {{c1::Vitamin B12 and B9 (folate)::2}}
Published	01/14/2024	Cystathionine beta synthase (CBS) deficiency results in high {{c1::homocysteine}} levels, increasing risk for thrombosis
Published	01/14/2024	Protein C and S normally {{c2::inactivate}} factors {{c1::Va}} and {{c1::VIIIa}}
Published	01/14/2024	{{c3::Protein C}} deficiency causes increased risk of {{c1::thrombotic skin necrosis}} with hemorrhage after {{c2::warfarin}} administration
Published	01/14/2024	In the initial stages of warfarin therapy, there is a temporary deficiency of {{c1::protein C}} compared to factors II, VII, IX, and X
Published	01/14/2024	{{c1::Factor V Leiden}} is a mutated form of factor V that is resistant to degradation by activated {{c2::protein C}}
Published	01/14/2024	Factor V Leiden is due to a point mutation near the {{c1::cleavage}} site of factor V
Published	01/14/2024	What point mutation is the cause of Factor V Leiden? {{c1::Arg506Gln (G -> A point mutation)}}
Published	01/14/2024	What is the most common inherited cause of hypercoagulable state in Caucasians? {{c1::Factor V Leiden}}
Published	01/14/2024	{{c2::Prothrombin 20210A}} is an inherited point mutation in the prothrombin gene that results in {{c1::increased}} gene expression
Published	01/14/2024	Prothrombin 20210 mutation is a point mutation in the {{c1::3' untranslated}} region of the gene
Published	01/14/2024	What drug enhances activity of antithrombin? {{c1::Heparin}}
Published	01/14/2024	What coagulation factors are inhibited by antithrombin? {{c1::2, 7, 9, 10, 11, 12::6}}
Published	01/14/2024	What coagulation factors are the principal targets of antithrombin? {{c1::IIa (thrombin) and Xa::2}}
Published	01/14/2024	What is the effect of oral contraceptives on coagulability? {{c1::Increases coaguability}}
Published	01/14/2024	What is the effect of estrogen on production of coagulation factors? {{c1::Increased production}}
Published	01/14/2024	Tissue plasminogen activator (tPA) may be administered clinically as a(n) {{c1::thrombolytic}}
Published	01/14/2024	The three major risk factors for thrombosis are {{c1::disruption in blood flow (stasis)}}, {{c2::hypercoagulability}}, and {{c3::endothelial cell dama…
Published	01/14/2024	What lab test is used clinically to rule out DVT (high sensitivity, low specificity)? {{c1::D-dimer}}
Published	01/14/2024	Pulmonary embolism may present with {{c1::elevated}} D-dimer
Published	01/14/2024	What effect do ACE inhibitors have on bradykinin activity?{{c1::Increased}}
Published	01/14/2024	{{c3::ACE}} inhibitors are contraindicated in patients with {{c1::hereditary angioedema}}, which is characterized by a(n) {{c2::C1 esterase inhib…
Published	01/14/2024	ACE inhibitors may cause angioedema due to increased {{c1::bradykinin}}
Published	01/14/2024	Intrarenal azotemia is less commonly due to acute {{c1::glomerulonephritis}} or acute {{c2::interstitial nephritis}}
Published	01/14/2024	Nephrotic syndrome causes a(n) {{c1::hyper}}-coagulable state due to loss of {{c2::antithrombin III}}
Published	01/14/2024	Uremia, a consequence of renal failure, may cause {{c1::platelet}} dysfunction in the blood
Published	01/14/2024	Vitamin C deficiency is characterized by a(n) {{c1::increased}} bleeding time
Published	01/14/2024	Vitamin {{c1::K}} injection is given at birth to prevent hemorrhagic disease of the newborn
Published	01/14/2024	Vitamin K deficiency may cause neonatal {{c1::hemorrhage}}
Published	01/14/2024	Vitamin K deficiency is characterized by a(n) {{c1::normal}} bleeding time
Published	01/14/2024	Vitamin K deficiency is characterized by a(n) {{c1::increased}} PT and {{c1::increased}} PTT
Published	01/14/2024	Vitamin K deficiency can occur after prolonged use of broad-spectrum {{c1::antibiotics}}
Published	01/14/2024	Microangiopathic hemolytic anemia (MAHA) is primarily characterized by {{c1::intravascular}} hemolysis
Published	01/14/2024	{{c1::Microangiopathic hemolytic}} anemia occurs due to damage of RBCs as they pass through obstructed or narrowed vessels (e.g. due to microthrombi)
Published	01/14/2024	What type of anemia is caused by TTP, HUS, DIC, and HELLP? {{c1::Microangiopathic hemolytic anemia}}
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