Exam 2

Question 1

Antihyperlipidemics

Answer 1

agents which decrease the concentration of circulating lipoproteins

Question 2

Least dense lipoproteins

Answer 2

Chylomicrons

Question 3

lipoproteins transform form of GI absorbed triglycerides

Answer 3

chylomicrons

rapidly removed from circulation into adipose tissue and skeletal muscle

Question 4

VLDL are synthesized in ___________.

Answer 4

liver

Question 5

Which lipoproteins transport lipids to peripheral tissues?

Answer 5

Very low density lipoproteins (VLDL)

Question 6

Which lipoproteins are the major transporter of cholesterol?

Answer 6

low density of lipoproteins (LDL)
bad lipoprotein

Question 7

Where are LDL’s synthesized?

Answer 7

liver

Question 8

Where are HDL synthesized?

Answer 8

liver

Question 9

Which lipoproteins are reverse cholesterol transporters (tissue to liver)?

Answer 9

High-density lipoproteins
“good” lipoprotein

Question 10

Atherosclerotic plaques develop with addition of:

Answer 10

Cholesterol
Calcium
Collagen
Fibrin

Question 11

High concentrations of ___________ lead to an increased risk of atherosclerosis based on the movement of “sticky” cholesterol to vessel walls and the build-up of plaques.

Answer 11

LDL

Question 12

Increased ratio of ____________ is considered desirable.

Answer 12

HDL: LDL

Question 13

Is dietary cholesterol the only source of body cholesterol?

Answer 13

no-liver synthesized cholesterol based on body levels.

Question 14

What levels of plasma concentration should be decreased in order to help lower cholesterol levels?

Answer 14

triglycerides because they are used to synthesize cholesterol

Question 15

Hyperlipidemia occurs in _____% of the population.

Answer 15

15-20%

Question 16

Risk factors of hyperlipidemia

Answer 16

PEGSS

Poor diet
Excessive alcohol consumption
Genetics
Smoking
Sedentary lifestyle

Question 17

Primary goal in treatment of hyperlipidemia

Answer 17

to lower LDL and triglycerides while increasing HDL/LDL ratio

Question 18

What is the first-line therapy in hyperlipidemia?

Answer 18

diet modification and excercise plans

-however, not likely to be extremely effective at lowering very high cholesterol and triglyceride levels
-diet rich in unsaturated fats decreases LDL and increases HDL

-drug therapy can be very effective and useful in most patients

Question 19

Which agents are recommended for use in patients with high LDL but near normal Triglyceride levels?

Answer 19

Bile acid binding resins

Question 20

Drugs that are bile acid binding resins

Answer 20

Cholestyramine (Questran)
Colestipol (Colestid)
Colesvelam (Welchol)

Question 21

are bile acid-binding resins water soluble?

Answer 21

no, water insoluble cation exchange resins that bind up released bile salts (and their attached cholesterol) in the GI tract and prevent their reabsorption

Question 22

Bile-Acid binding resins result in a ________% decrease in circulating LDL cholesterol (plasma triglycerides may increase due to increased hepatic LDL receptors and increased LDL catabolism.

Answer 22

30%

Question 23

Bile-acid binding resins adverse effects

Answer 23

-constipation
-poor compliance (sand-like consistency)
-abdominal cramping
-absorption of fat-soluble vitamins
-may bind to several other drugs (ex. digitalis, beta-blockers etc.) so separate doses

Question 24

What are considered first-line antihyperlipidemics ?

Answer 24

bile acid binding resins

Question 25

What is the MOA of HMG-CoA reductase inhibitors (Statins)?

Answer 25

inhibit the rate-limiting enzyme in cholesterol synthesis (3-hydroxy-3-methylglutaryl coenzyme A reductase) -therefore block cholesterol synthesis (not dietary) and decrease LDL cholesterol. -decreased LDL levels also stimulate the production of hepatic LDL receptors and thus further decreases the plasma LDL level -all act in primarily in the liver to decrease production of cholesterol

Question 26

Statins are considered first-line therapeutics, however their side effect profile is _______________ than bile acid binding resins.

Answer 26

greater

Question 27

HMG CoA reductase inhibitor drugs

Answer 27

-Lovastatin -Atorvastatin (lipitor) -Fluvastatin (Lescol) -Pravastatin (Pravachol) -Simvastatin (Zocor) -Rosuvastatin (Crestor) -Pitavastatin (Livalo)

Question 28

Which agents are very useful in cases of genetic hypercholesterolemia?

Answer 28

HMG-CoA reductase inhibitors

Question 29

Which antihyperlipidemics should be avoided in pregnancy?

Answer 29

HMG-CoA reductase inhibitors

Question 30

Statins decrease plasma cholesterol by up to ____% and decrease triglyceride levels by _______%.

Answer 30

30% 10-20%

Question 31

Statins have a ________ (high or low) first-pass effect.

Answer 31

high

Question 32

Adverse effects of Statins

Answer 32

-may increase plasma aminotransferase levels (d/c if levels increase more than 3x normal) -skeletal muscle weakness/pain -linked to increased plasma creatinine phosphokinase -may become severe leading to rhabdomyolysis and renal failure -more common when taking certain drugs such as macrolide Abx and antifungal agents - effects may be less with Flubastatin -Rosuvastatin may be more likely to cause

Question 33

Which medication should be avoided in patients taking Statins?

Answer 33

Sux unless absolutely necessary -linked use of Sux in patients taking statins with increased risks of muscle pain and injury up to rhabdomyolysis and related kidney damage

Question 34

How are Statins metabolized?

Answer 34

partly CYP3A4

Question 35

Which statin is metabolized by CYP2C9 which is not affected by grapefruit juice?

Answer 35

Pitavastatin

Question 36

How does grapefruit juice affect statins?

Answer 36

-grapefruit juice contains compounds (furanocoumarins) which inhibit CYP3A4 thus increasing duration of many statins and possibly leading to increased risk of rhabdo or other myopathy and muscle pain -especially seen with SAL :) -Simvastatin -Atorvastatin -Lovastatin

Question 37

MOA of Niacin (Nicotinic Acid)

Answer 37

-decreases both VLDL and LDL plasma levels -mech unclear, believed to act by increasing VLDL clearance and decreasing VLDL synthesis which then leads to decrease in conversion to LDL -inhibits free fatty acid release from adipose tissue

Question 38

Niacin can lower LDL by ____ with up to a _______ decrease in triglycerides.

Answer 38

30% 50%

Question 39

Niacin increased HDL levels ______%

Answer 39

20-30%

Question 40

Adverse effects of Niacin

Answer 40

-benefits closely linked to dose, higher doses not well tolerated -large doses can lead to hepatic damage, which is believe to be due to a direct hepatic effect -hyperglycemia -increased plasma uric acid levels -potent vasodilator, which leads to flushing, headaches and potential orthostatic hypotension and syncope -flushing (and pruritus) is prostaglandin mediated and can be avoided by pretreatment with aspirin -abdominal pain and diarrhea -increased risk of skeletal muscle myopathy when given with HMG-CoA reductase inhibitors.

Question 41

What are the fibrate drugs?

Answer 41

Fenofibrate Gemfibrozil Clofibrate

Question 42

MOA of Gemfibrozil (Lopid)

Answer 42

-stimulation of lipoprotein lipases which break down triglycerides -used mainly to treat patients with increased triglycerides without increased LDL cholesterol

Question 43

Gemfibrozil (Lopid) lowers triglycerides up to _____% and increase HDL up to____%.

Answer 43

50% 20%

Question 44

How is Gemfibrozil eliminated?

Answer 44

renal in unchanged form, care in renal compromised patients

Question 45

Adverse effects of Gemfibrozil

Answer 45

-small increase in patient development of gallstones -increased risk of skeletal muscle myopathy, esp administered with Statins -GI upset -Arrythmias are possible and so should not be used in patient with a history of heart disease

Question 46

How do fenofibrates effect levels?

Answer 46

-more effective at lowering triglycerides than cholesterol -increases HDL cholesterol somewhat but not very effective at lowering LDL cholesterol

Question 47

Ezetimibe (Zetia) MOA

Answer 47

-different than other agents -inhibitor of intestinal cholesterol transport -does not inhibit liver synthesis of cholesterol or increase biliary excretion -reduces LDL cholesterol while increasing HLD cholesterol in patients with hypercholesterolemia

Question 48

Metabolism of Ezetimibe (Zetia)

Answer 48

liver glucuronidation then excreted in urine unchanged form excreted primarily in feces enterohepatic recycling occurs

Question 49

t1/2 of Ezetimibe

Answer 49

22 hours

Question 50

Which med is recommended only when other agents either are not effective or tolerated but to controversy concerning true effectiveness?

Answer 50

Ezetimibe (Zetia)

Question 51

PCSK9 inhibitor drugs

Answer 51

Alirocubmab (Praluent) Evolocumab (Repatha)

Question 52

When were PCSK9 inhibitors approved?

Answer 52

2015 newest class for lowering cholesterol

Question 53

How do PCSK99 inhibitors work?

Answer 53

-monoclonal antibodies which inhibit human proprotein convertase subtilisin kexin 9 binding to liver LDL receptors allowing more LDL particles to be reabsorbed by the liver and decrease circulating LDL

Question 54

Which agents are for patients no able to take other antihypercholesterolemics or other agents are not working?

Answer 54

PCSK9 inhibitors

Question 55

Which med is a prodrug activated by coenzyme A which inhibits adenosine triphosphate citrate lyase in liver?

Answer 55

Bempedoic acid (NExletol) enzyme is needed for cholesterol synthesis

Question 56

which drug was approved for use in familial hypercholesterolemia in combination with statin therapy and dietary control?

Answer 56

Bempedoic acid (Nexletol) -not first line therapy

Question 57

Side effects of Bempedoic acid

Answer 57

-muscle spasms, back and limb pain , gout, diarrhea -more serious SE include tendon rupture (0.5%) -weak transport protein inhibition may account for increased gout attacks and increased blood statin levels (simvastatin and pravastatin mainly)

Question 58

Withold ______ during perioperative period. Can decrease platelet counts and increase prothrombin time.

Answer 58

Niacin

Question 58

Which med caused cutaneous and peripheral vasodilation (flushing) which can lead to hypotension with general anesthetics.

Answer 58

Niacin

Question 59

Which agents have higher risk of rhabdomyolysis than the statins in hospitalized patients and should be d/c'd prior to surgery?

Answer 59

fibrates

Question 60

Antiplatelet drugs action

Answer 60

to decrease plt aggregation and formation of a plt plug

Question 61

Anticoagulants inferfere with the____________.

Answer 61

coagulation cascade, thus blocking thrombus formation

Question 62

How is the platelet plug strengthened?

Answer 62

addition of fibrin to form a cross-linked matrix via the coagulation cascade

Question 63

Platelets contain mainly ______ and since they do not contain _____ they cannot synthesize additional _______.

Answer 63

cox-1 DNA COX

Question 64

How does high intracellular cAMP levels interfere with platelet aggregation?

Answer 64

high CaMP inhibits aggregation

Question 65

How do low intracellular cAMP levels interfere with platelet aggregation?

Answer 65

low CaMP enhance aggregation

Question 66

cAMP levels are controlled by ______.

Answer 66

TX-A2 (and other mediators)

Question 67

Dipyridamole (Persantine) is a _______ inhibitor.

Answer 67

PDE-5 inhibitor, however it is only weakly antiplatelet and usually given with warfarin to decrease thrombus formation in heart valve replacement or with aspirin.

Question 68

What can dipyridamole (Persantine) induce?

Answer 68

angina in susceptible patients due to a vasodilatory property which can increase cardiac steal.

Question 69

Which are prodrugs that are activated in the liver and covalently bind to the P2Y12 receptor protein, decreasing platelet aggregation?

Answer 69

Clopidogrel (plavix) Ticlodipine

Question 70

Uses of Ticlodipine

Answer 70

decreases embolus risk after coronary stent placement and use in patients who cannot tolerate aspirin

Question 71

Uses of Clopidogrel

Answer 71

-prevent secondary MI, Stroke, PVD, bypass graft surgery

Question 72

How is Cangrelor (Kengreal) different than Clopidogrel?

Answer 72

it is an active compound so does not require metabolic activation -it is an IV agent that has been shown to decrease mortality when used with Clopidogrel in CV stent placement in MI patients

Question 73

What is an oral P2Y12 irreversible inhibitor used to decrease clotting risks in CV stent patients?

Answer 73

Prasugrel (Effient) -similar to Clopidogrel -used with low dose aspirin

Question 74

What is a oral P2Y12 reversible inhibitor?

Answer 74

Ticagrelor (Brilinta) acts on a different site and produces an allosteric change blocking ADP binding -CYP3A4 inhibitors (grapefruit juice, ketoconazole etc) can lead to increased risk of excessive bleeding

Question 75

What is considered the final pathway in aggregation?

Answer 75

glycoprotein IIb/IIIa receptor GPIIb/IIIa receptors on platelet surface is the location that binds fibrinogen allowing platelets to bind together during aggregation. Blocking this binding site keeps platelets from aggregating

Question 76

What are the glycoprotein IIb/IIIa receptor antagonists

Answer 76

-Abciximab (reopro) -eptifabatide (Integrilin) -Tirofiban (aggrastat)

Question 77

Which Glycoprotein IIB/IIIa receptor antagonist is a monoclonal antibody for IV use?

Answer 77

Abciximab (reopro)

Question 78

What is the t1/2 of Abciximab?

Answer 78

12-24 hours affinity for receptor very strong (almost irreversible) -recommend with aspirin or warfarin to decrease SE risk

Question 79

How do you reverse Abciximab?

Answer 79

with platelet infusions

Question 80

Which Glycoprotein IIB/IIIa receptor antagonist is a synthetic peptide with a high affinity but shorter t1/2 (2-4 hours) than Abciximab?

Answer 80

Eptifibatide (Integrilin)

Question 81

Which Glycoprotein IIB/IIIa receptor antagonist is a non-peptide tyrosine analog with t1/2 2-4 hours?

Answer 81

Tirofiban (Aggrastat)

Question 82

Which anticoags are useful for arterial and venous thrombotic disease?

Answer 82

Thrombin inhibitors

Question 83

Which are the Thrombin inhibitors?

Answer 83

-Bivalrudin (Angiomax) -Argatroban (Acova) -Dabigatran (Pradaxa) -Lepirudin -Recombinant Hirudin

Question 84

What are the ADP inhibitors?

Answer 84

also known as P2y12 inhibitors: Clopidogrel (Plavix) Prasugrel (Effient) Ticagrelor (Brillinta) Ticlodipiine (Ticlid)

Question 85

Which thrombin inhibitors can be used as a heparin replacement in patients not responding to heparin or experiencing heparin-induced thrombocytopenia?

Answer 85

Recombinant Hirudin (Desirudin)

Question 86

Which thromin inhibitor is a peptide that directly inhibits thrombin without the need of antithrombin that heparin requires?

Answer 86

recombinant hirudin

Question 87

Which is a synthetic peptide similar to Hirudin?

Answer 87

Bivalrudin (Angiomax)

Question 88

Which is a arginine derivative used in place of heparin that is a thrombin inhibitor?

Answer 88

Argatroban (acova) in addition to its direct thrombin inhibition, it triggers nitric oxide release which increases perfusion in peripheral vascular disease

Question 89

Where is heparin found?

Answer 89

in mast cell and nerve terminal vesicles

Question 90

What is heparin structurally?

Answer 90

strongly acidic glycosaminoglycan of high molecular weight chains with 10-100 monosaccharide residues

Question 91

Heparin is _______ at physiologic pH , which explains most SE.

Answer 91

polyanionic

Question 92

What does heparin require for action?

Answer 92

a cofactor-->antithrombin III

Question 93

What factors does Heparin inhibit?

Answer 93

Coag factors: IXa Xa XIa XIIa thrombin activity

Question 94

Heparin metabolism

Answer 94

50% metabolized 50% eliminated unchanged in the urine

Question 95

t1/2 heparin

Answer 95

1-2 hours increases dramatically in liver or renal disease

Question 96

Can heparin be given in pregnancy?

Answer 96

yes, fairly safe since it does not cross placenta

Question 97

Heparin activity is due to a specific _________________ sequence.

Answer 97

pentasaccharide

Question 98

Heparin effects can be immediately reversed with _________ which is a _____________.

Answer 98

Protamine ionic binder

Question 99

Low-molecular weight heparins

Answer 99

Enoxaparin (Lovenox) Dalteparin (Fragmin)

Question 100

How is low-molecular weight heparin produced?

Answer 100

by cleavage of heparin into smaller polysaccharide chains -all have the specific pentasaccharide required for activity like heparin -more bioavailable than Heparin when given SQ

Question 101

Why do LMWH decrease side effects?

Answer 101

less binding to cells and other proteins due to lower overall charge

Question 102

Which anticoagulant acts with antithrombin to inhibit factor Xa but not thrombin?

Answer 102

Fondaparinux (Arixtra)

Question 103

Warfarin administration should be d/c'd how many days prior to surgery?

Answer 103

2-5 days

Question 104

What can be given to reverse effects of warfarin if needed for emergency surgery?

Answer 104

Vitamin K or FFP to provide prothrombin

Question 105

Warfarin clearance rate is decreased with:

Answer 105

Amiodarone Cimetadine Omeprazole

Question 106

Should Warfarin be avoided in pregnancy?

Answer 106

Yes! crosses placenta into fetus and produces exaggerated actions in fetus

Question 107

How do oral anticoagulants such as warfarin work?

Answer 107

-act as competitive inhibitors of Vitamin K, which is needed for synthesis of prothrombin -therefore they decrease the amount of prothrombin available to be converted to thrombin by factor Xa -due to this mechanism, these agents have fairly slow onsets (24-48 hours) and long durations (2-5 days_

Question 108

Thrombin converts _______ to ________ which are crosslinked by factor _____ to form thrombotic web.

Answer 108

fibrinogen to fibrin crosslinked by factor XIIIa

Question 109

Is Dabigatran considered safer than warfarin?

Answer 109

yes

Question 110

Which oral anticoagulant is an esterase prodrug form activated by plasma and liver esterases?

Answer 110

dabigatran (Pradaxa) -binds to bound free and clot-found thrombin

Question 111

How is Dabigatran metabolized and excreted?

Answer 111

80% renally excreted remainer metabolized by liver

Question 112

D/C Rivaroxaban (Xarelto) _______ hours prior to surgery?

Answer 112

24-48 hours

Question 113

D/C Apixaban (Eliquis) _______ hours prior to surgery?

Answer 113

24-48 hours

Question 114

D/C Edoxaban (savaysa) _______ hours prior to surgery?

Answer 114

24-48 hours

Question 115

What newer oral anticoagulants is a new variant of factor Xa inhibitors specifically approved for hospitalized and transitioning patients to prevent DVT And VTE formation?

Answer 115

Betrixaban (Bevyxxa) -d/cd by manufacturer in 2020 prior to corporate buy-out

Question 116

Which drug is a recombinant product to reverse factor Xa inhibotrs?

Answer 116

Adexanet alfa (Andexxa) effective but very expensive :25k

Question 117

Thrombolytic agents MOA

Answer 117

-used to dissolve formed clot -primary indication is emergency tx of a coronary occlusion -convert plasminogen to plasmin which is an enzyme responsible for cleaving fibrin molecules, thus breaking apart the 'web' matrix of a thrombus recommended in patients within 12 hours of onset of MI symptoms with ST segment elevation

Question 118

Thrombolytic agents (drugs)

Answer 118

Streptokinase (Streptase) Alteplase (Activase)

Question 119

Which thrombolytic agent is isolated from beta-hemolytic streptococci?

Answer 119

Streptokinase (Streptase) -acts by binding to plasminogen causing other molecules to be converted to plasmin which then breaks down fibrin -allergic reactions possible in patients who have been exposed to beta-hemolytic streptococcal infections

Question 120

Which is a recombinant form of tissue plasminogen activator?

Answer 120

Alteplase (Activase) more expensive than streptokinase

Question 121

Blood composition

Answer 121

92% water 8% solutes

Question 122

Plasma is _______ % of blood volume

Answer 122

50-55%

Question 123

What is serum?

Answer 123

plasma that has been allowed to clot to remove fibrinogen (may interfere with diagnostic tests)

Question 124

polycythemia

Answer 124

too many cells

Question 125

anemia

Answer 125

too few cells -reduction in the total number of erythrocytes in circulating blood or in the quality or quantity of hemoglobin

Question 126

Causes of anemia:

Answer 126

-impaired erythrocyte production -acute or chronic blood loss -increased erythrocyte destruction -combination of above

Question 127

Classification of anemia

Answer 127

-etiologic factor(cause) -size identified by terms that end in 'cytic" macrocytic (large) microcytic (Small) normocytic (normal) -hemoglobin content -identified in terms that end in "chromic" -hypochromic (decreased amount)

Question 128

Anisocytosis

Answer 128

-RBC are present in various sizes

Question 129

Poikilocytosis

Answer 129

RBCs present in various shapes

Question 130

Clniical manifestations of anemia

Answer 130

-reduced O2 carrying capacity: hypoxia -snycope, angina, compensatory tachycardia, and Jordan dysfunctions Classic anemia symptoms: -fatigue -weakness -dyspnea -elevated HR -pallor

Question 131

Treatment of anemia

Answer 131

-transfusions -dietary correction -administration of supplemental vitamins or iron -correction of underlying condition

Question 132

What are macrocytic-normochromic anemias also termed?

Answer 132

Megaloblastic anemias

Question 133

What is the patho of macrocytic-normochromic anemia?

Answer 133

RBCs are unusually large. Deoxyribonucleic acid (DNA) synthesis is defective. Due to deficiencies in vitamin B12 or folate. Co-enzymes for nuclear maturation and the DNA synthesis pathway Ribonucleic acid (RNA) processes occur at a normal rate. Results in unequal growth of the nucleus and cytoplasm.

Question 134

What is the most common macrocytic anemia?

Answer 134

Pernicious anemia

Question 135

What is pernicious anemia caused by?

Answer 135

vitamin B12 deficiency -lacks intrinsic factor from gastric parietal cells required for vitamin B12 absorption -may be a congenital or autoimmune disorder -autoantibodies against intrinsic factor

Question 136

Conditions that increase risk of pernicious anemia

Answer 136

-past infection with Helicobacter pylori -gastrectomy -proton-pump inhibitors

Question 137

Clinical manifestations of pernicious anemia

Answer 137

-weakness, fatigue -paresthesias of feet, fingers, difficulty walking -loss of appetite, abdominal pain, weight loss -sore tongue that is smooth and beefy red, secondary to atrophic glossitis -"lemon yellow" (sallow) skin as a result of a combo of pallor and icterus -neuro symptoms from nerve demyelination-not reversible even with tx -often unrecognizable in older adults because of its subtle slow onset and presentation

Question 138

Evaluation of pernicious anemia

Answer 138

-methylmalonic acid and homocysteine levels elevated early in disease -gastric bx

Question 139

Treatment of pernicious anemia

Answer 139

-parenteral or high oral doses of vitamin B12 -if left untreated,death -life-long tx required

Question 140

What is folate deficiency anemia?

Answer 140

Folate is an essential vitamin for RNA and DNA synthesis. Absorption of folate occurs in the upper small intestine; is not dependent on any other facilitating factors.

Question 141

folate deficiency anemia is common in:

Answer 141

Is common in alcoholics and individuals with chronic malnourishment.

Question 142

Folate deficiency anemia is associated with what in fetus?

Answer 142

neural tube defects

Question 143

Clinical manifestations of folate deficiency anemia

Answer 143

Severe cheilosis: Scales and fissures of the lips and corners of the mouth Stomatitis: Mouth inflammation Painful ulcerations of the buccal mucosa and tongue: Characteristic of burning mouth syndrome Dysphagia (difficulty swallowing), flatulence, and watery diarrhea Neurologic symptoms: Usually not seen

Question 144

Treatment of folate deficiency

Answer 144

Oral dose of folate is administered daily until normal blood levels are obtained. Life-long treatment is not necessary.

Question 145

causes of microcytic-hypochromic anemias

Answer 145

Disorders of iron metabolism Disorders of porphyrin and heme synthesis Disorders of globin synthesis

Question 146

Microcytic-hypochromic anemia characterized by:

Answer 146

Are characterized by RBCs that are abnormally small and contain reduced amounts of hemoglobin

Question 147

Most common type of anemia worldwide

Answer 147

iron-deficiency anemia

Question 148

Highest risk of iron deficiency anemia

Answer 148

Older adults, women, infants, and those living in poverty

Question 149

Which anemia is associated with cognitive impairment in children

Answer 149

iron deficiency anemia

Question 150

Causes of iron deficiency anemia

Answer 150

Inadequate dietary intake Excessive blood loss Chronic parasite infestations Metabolic or functional iron deficiency Menorrhagia (excessive bleeding during menstruation) Use of medications that cause gastrointestinal bleeding (aspirin, nonsteroidal antiinflammatory drugs [NSAIDs]) Surgical procedures that decrease stomach acidity, intestinal transit time, and absorption (e.g., gastric bypass) Insufficient dietary intake of iron Eating disorders, such as pica (craving and eating nonnutritional substances such as dirt, chalk, and paper)

Question 151

Clinical manifestations of iron-deficiency anemia

Answer 151

Fatigue, weakness, shortness of breath Pale earlobes, palms and conjunctivae Brittle, thin, coarsely ridged, and spoon-shaped (concave or koilonychia) nails Red, sore, painful tongue Angular stomatitis: Dryness and soreness in the corners of the mouth Become symptomatic: When hemoglobin (Hgb) 7 to 8 g/dl

Question 152

Tx of iron-deficiency anemia

Answer 152

Iron replacement therapy: Iron dextran Sodium ferric gluconate complex in sucrose (Ferrlecit) and iron sucrose injection (Venofer) Duration of therapy: Usually 6 to 12 months after the bleeding has stopped but may continue for as long as 24 months

Question 153

Evaluation of iron-deficiency anemia

Answer 153

serum ferritin

Question 154

What is sideroblastric anemia?

Answer 154

Makes up a group of disorders characterized by anemia. Is caused by a defect in mitochondrial heme synthesis. Altered mitochondrial metabolism causes ineffective iron uptake and results in dysfunctional hemoglobin synthesis. Ringed sideroblasts in the bone marrow are diagnostic. Sideroblasts: Erythroblasts contain iron granules that have not been synthesized into hemoglobin.

Question 155

What are the clinical manifestations of sideroblastic anemia?

Answer 155

Iron overload (hemochromatosis) Enlarged spleen (splenomegaly) and liver (hepatomegaly)

Question 156

Evaluation of sideroblastic anemia

Answer 156

Bone marrow examination: Diagnostic Dimorphism: Normocytic and normochromic cells concomitantly observed with microcytic-hypochromic cells

Question 157

Reversible sideroblastic anemia associated with

Answer 157

alcoholism

Question 158

Treatment of sideroblastic anemia

Answer 158

Identify causative agents (drugs or toxins) Transfusion Iron-depletion therapy Phlebotomy Prolonged administration of erythropoietin Hereditary: Pyridoxine (B6) therapy; life-long maintenance therapy at a lowered dose Congenital: Stem cell transplantation Myelodysplastic syndrome: Recombinant human erythropoietin

Question 159

Normocytic-normochromic anemia

Answer 159

Are characterized by RBCs that are relatively normal in size and hemoglobin content but insufficient in number. No common cause, pathologic mechanisms, or morphologic characteristics exist. Are less frequent than macrocytic-normochromic and microcytic-hypochromic anemias.

Question 160

Pancytopenia

Answer 160

reduction or absence of all three types of blood cells

Question 161

Pure RBC aplasia

Answer 161

only RBCs affected

Question 162

Faconi anemia

Answer 162

rare genetic anemia from defects in DNA repair

Question 163

Clinical manifestations of aplastic anemia

Answer 163

Hypoxemia, pallor (occasionally with a brownish pigmentation of the skin) Weakness along with fever and dyspnea with rapidly developing signs of hemorrhaging if platelets are affected

Question 164

Patho of aplastic anemia

Answer 164

Hypocellular bone marrow that has been replaced with fat

Question 165

Evaluation of aplastic anemia

Answer 165

bone marrow bx

Question 166

Tx of aplastic anemia

Answer 166

Bone marrow transplantation Peripheral blood stem cell transplantation May receive radiation or chemotherapy before procedure Immunosuppression Antithymocyte globulin with cyclosporin Corticosteroidal medications Identification of high-risk individuals If not treated or identified, death occurs

Question 167

Post-hemorrhagic anemia

Answer 167

Acute blood loss from the vascular space Clinical manifestations Depends on the severity of the blood loss Treatment Intravenous administration of saline, dextran, albumin, or plasma Large volume losses: Fresh whole blood

Question 168

Clinical manifestations of hemolytic anemia

Answer 168

May be asymptomatic Jaundice (icterus) Splenomegaly

Question 169

Evaluation of hemolytic anemia

Answer 169

Bone marrow: Abnormally increased numbers of erythrocyte stem cells (erythroid hyperplasia)

Question 170

Tx of hemolytic anemia

Answer 170

Acquired: Removal of the cause or treatment of the underlying disorder First line: Corticosteroids Second line: Splenectomy and Rituximab (Rituxan) (monoclonal antibody) Paroxysmal nocturnal hemoglobinuria: Eculizumab (Solaris)

Question 171

Pathologic mechanisms of anemia

Answer 171

Decreased erythrocyte lifespan Suppressed production of erythropoietin Ineffective bone marrow response to erythropoietin Altered iron metabolism

Question 172

Relative polycythemia

Answer 172

Is a result of dehydration. Fluid loss results in relative increases of RBC counts and hemoglobin and hematocrit values. Resolves with fluid intake.

Question 173

Polycythemia

Answer 173

overproduction of RBCs

Question 174

Paroxysmal nocturnal hemoglobinuria

Answer 174

Deficiency in CD55 and CD59: Cause complement-mediated intravascular lysis and release of hemoglobin Anemia, hemoglobinuria, severe fatigue, abdominal pain, and thrombosis

Question 175

Autoimmune hemolytic anemia

Answer 175

Autoantibodies against antigens normally on the surface of erythrocytes

Question 176

Drug induced hemolytic anemia

Answer 176

Form of immune hemolytic anemia that is usually the result of an allergic reaction against foreign antigens Called the hapten model Penicillin, cephalosporins (more than 90%), hydrocortisone

Question 177

Disease leading to anemia of chronic disease

Answer 177

-AIDS -Malaria -RA -Lupus -Hepatitis -Renal Failure -Malignancies

Question 178

Polycythemia Vera

Answer 178

Chronic neoplastic, nonmalignant condition Overproduction of RBCs (frequently with increased levels of WBCs [leukocytosis] and platelets [thrombocytosis]) Splenomegaly

Question 179

Patho of Polycythemia vera

Answer 179

Is an acquired mutation in Janus kinase 2 (JAK2). Negates the self-regulatory activity of JAK2 that allows the erythropoietin receptor to be constitutively active, regardless of the level of erythropoietin. Disease can convert into acute myeloid leukemia.

Question 180

Polycythemia vera s/s

Answer 180

Spleen becomes enlarged, frequently with abdominal pain and discomfort. As the disease progresses, blood cellularity and viscosity increases. Intense, painful itching is intensified by heat or exposure to water (aquagenic pruritus

Question 181

Treatment of polycythemia vera

Answer 181

Phlebotomy: Withdrawal of 300 to 500 ml of blood at a time to reduce erythrocytosis and blood volume Low-dose aspirin Interferon-α Hydroxyurea Radioactive phosphorus

Question 182

Hereditary Hemochromatosis

Answer 182

Common inherited, autosomal recessive disorder of iron metabolism Characterized by increased gastrointestinal iron absorption with subsequent tissue iron deposition Excess iron deposited in the liver, pancreas, heart, joints, and endocrine gland, causing tissue damage

Question 183

s/s of hereditary hemochromatosis

Answer 183

Fatigue, malaise Abdominal pain, arthralgias, and impotence Hepatomegaly, abnormal liver enzymes, bronzed skin, diabetes, and cardiomegaly

Question 184

Treatment of Hereditary hemochromatosis

Answer 184

Phlebotomy; refrain from taking iron and vitamin C supplements and consuming raw shellfish; alcohol use in moderation

Question 185

What are the myeloproliferative RBC disorders?

Answer 185

1. Polycythemia vera 2. Relative Polycythemia 3. Hereditary Hemochromatosis (iron overload)

Question 186

Quantitative disorders of leukocyte function

Answer 186

-Increases or decreases in cell numbers -Bone marrow dysfunction or premature destructionof cells -Response to infectious microorganism invasion

Question 187

Qualitative disorders of leukocytes

Answer 187

Disruption of leukocyte function Phagocytic cells (granulocytes, monocytes, macrophages) may lose their phagocytic capacity to function. Lymphocytes may lose their capacity to respond to antigens.

Question 188

Leukocytosis

Answer 188

-Counts are higher than normal. -Is a normal protective physiologic response to stressors or to the invasion of microorganisms. -Can be pathological

Question 189

Leukopenia

Answer 189

Counts are lower than normal. Is always abnormal. Low white blood cell (WBC) count predisposes a person to infections.

Question 190

What is evident in the first stages of infection or inflammation?

Answer 190

Granulocytosis (Neutrophilia) -If the need for neutrophils increases beyond the supply, then immature neutrophils (banded neutrophils) are released into the blood. -Premature release of immature leukocytes is termed a shift-to-the-left-producing more of precursor cells (bands or stabs) Leukemoid reaction

Question 191

Causes of Neutropenia

Answer 191

-Prolonged severe infection -Decreased production -Reduced survival -Abnormal neutrophil distribution and sequestration

Question 192

Congenital Neutropenia

Answer 192

Cyclic neutropenia and neutropenia with congenital immunodeficiency diseases Multiple syndromes

Question 193

Acquired neutropenia

Answer 193

Multiple conditions (hypoplastic anemia, aplastic anemia, leukemias, lymphomas [Hodgkin, non-Hodgkin]; myelodysplastic syndrome)

Question 194

Secondary Neutropenia

Answer 194

Lower count from other disorders (e.g., immune disorders and drugs); toxin, drug or environmental

Question 195

Causes of Granulocytopenia (Agranulocytosis)

Answer 195

-Interference with hematopoiesis -Immune mechanisms -Chemotherapy destruction -Ionizing radiation

Question 196

Eosinophilia

Answer 196

-eosinophil count increased -hypersensitivty reactions trigger release of eosinophilic chemotactic factor or anaphylaxis from mast cells

Question 197

Causes of Eosinophilia

Answer 197

-allergic disorders -parasitic invasions

Question 198

Eosinopenia

Answer 198

eosinophil count decreased

Question 199

Primary cause of eosinopenia

Answer 199

-migration of cells to inflammatory sites

Question 200

Other causes of eosinopenia

Answer 200

-Surgery -Shock -Trauma -Burns -Mental distress

Question 201

Basophilia

Answer 201

-Circulating numbers of basophils increase. -Occurs in inflammation and hypersensitivity reactions. -Contain histamine that is released in allergic reactions

Question 202

BAsopenia

Answer 202

-Circulating numbers of basophils decrease. -Occurs in acute infections, hyperthyroidism, and long-term steroid therapy

Question 203

Monocytosis

Answer 203

-Numbers of circulating monocytes increase. -Usually occurs with neutropenia in later stages of bacterial infections. -Found in chronic infection and correlates with extent of myocardial damage.

Question 204

Monocytopenia

Answer 204

-Numbers of circulating monocytes decrease. -Very little is known about this condition. causes: Prednisone treatments Hairy cell leukemia

Question 205

Lymphocytosis

Answer 205

-Circulating lymphocytes increase. -Occurs from acute viral infections Epstein-Barr virus (EBV) -Other causes Leukemia, lymphomas, some chronic infections

Question 206

Lymphocytopenia

Answer 206

Circulating lymphocyte counts decrease. Occurs from immune deficiencies, drug destruction, viral destruction, radiation, or acquired immunodeficiency syndrome (AIDS)

Question 207

Infectious Mononucleousis

Answer 207

Acute, self-limiting viral infection of B lymphocytes Commonly caused by the EBV—85% Transmission: Usually by saliva through personal contact (e.g., kissing, hence the term kissing disease)

Question 208

Clinical manifestations of Infectious Mononucleosis

Answer 208

Malaise, arthralgia Classic triad of symptoms: Fever Pharyngitis lymphadenopathy of the cervical lymph nodes

Question 209

Diagnostic test for infectious mononucleosis

Answer 209

Monospot qualitative test for heterophilic antibodies

Question 210

Treatment of infectious mononucleosis

Answer 210

Rest and alleviation of symptoms with analgesics and antipyretics and penicillin or erythromycin-takes about 6 weeks to clear Ibuprofen, not aspirin, for children and adolescents because of reported incidence of Reye syndrome

Question 211

Leukemias

Answer 211

Are malignant disorders of the blood and blood-forming organs. Exhibit uncontrolled proliferation of malignant leukocytes. Overcrowding of bone marrow Decreased production and function of normal hematopoietic cells Classification Predominant cell of origin: Myeloid or lymphoid Rate of progression: Acute or chronic

Question 212

Acute leukemia

Answer 212

Presence of undifferentiated or immature cells, usually blast cells Rapid onset with short survival

Question 213

Chronic Leukemia

Answer 213

Predominant cell is mature but does not function normally Slow progression

Question 214

Risk Factors of Leukemia

Answer 214

-Cigarette smoking, exposure to benzene, and ionizing radiation Human immunodeficiency virus (HIV), hepatitis C, human -T-lymphotropic virus type 1 (HTLV-1) -Drugs that cause bone marrow depression-chemotherapeutic drugs

Question 215

Pancytopenia

Answer 215

reduction in all cellular components of the blood

Question 216

What is the most common childhood leukemia?

Answer 216

acute lymphocytic leukemia (ALL) greater than 30% lymphoblasts in bone marrow or blood

Question 217

What is the cause of ALL?

Answer 217

Genetic anomaly: Philadelphia chromosome Reciprocal translocation (portion of one chromosome gets transferred to another chromosome and they swap) results in abnormal chromosome. Occurs between chromosomes 9 and 22.

Question 218

Risk factors of ALL

Answer 218

Prenatal x-ray exposure Postnatal exposure to high-dose radiation Viral infections with HTLV-1: Can cause a rare form of ALL and EBV Down syndrome

Question 219

What is the most common adult leukemia?

Answer 219

acute Myelogenous leukemia (AML) mean age, 67 years Down syndrome increases risk

Question 220

AML results from

Answer 220

-Abnormal proliferation of myeloid precursor cells -Decreased rate of apoptosis- -Arrest in cellular differentiation -Mutation in the receptor tyrosine kinase FLT3

Question 221

Risk factors of AML

Answer 221

Exposure to radiation, benzene, and chemotherapy Hereditary conditions

Question 222

Clinical manifestations o Leukemia

Answer 222

-Fatigue caused by anemia -Bleeding resulting from thrombocytopenia (reduced -numbers of circulating platelets) -Fever caused by infection -Anorexia, weight loss, diminished sensitivity to sour and sweet tastes, wasting away of muscle, and difficulty swallowing -Central nervous system (CNS) involvement

Question 223

Treatment of Leukemia

Answer 223

Chemotherapy Supportive measures Blood transfusions, antibiotics, antifungals, antivirals Allopurinol: Prevents the production of uric acid (which is elevated from cellular death because of treatment)-killing of cells can lead to build up of purines leading to increased uric acid Stem cell transplantation Bone marrow transplant

Question 224

Complications of Leukemia

Answer 224

Anemia Treatment: Blood products Neutropenia Treatment: Granulocyte colony-stimulated factor (G-CSF) or granulocyte-macrophage colony stimulating factor (GM-CSF) Low WBC count Treatment: Colony-stimulating factors to prevent infections

Question 225

Chronic myelogenous Leukemia (CML)

Answer 225

Is usually diagnosed in adults. Is a myeloproliferative disorder that also includes polycythemia vera, primary thrombocytosis, and idiopathic myelofibrosis. Philadelphia chromosome is often present and BCR-ABL1 causes initiation of CML

Question 226

Chronic Lymphocytic Leukemia (CLL)

Answer 226

Affects monoclonal B lymphocytes. Has a familial tendency.-genetic component Is common in adults older than 50 years.

Question 227

Clinical manifestations of CLL

Answer 227

Is asymptomatic at the time of diagnosis. Lymphadenopathy is the most common finding. Suppresses humoral immunity, and increases infection with encapsulated bacteria.

Question 228

CML phases

Answer 228

Infections, fever, and weight loss Chronic phase Lasts 2 to 5 years Symptoms: May not be apparent Accelerated phase Lasts 6 to 18 months Primary symptoms develop: Splenomegaly-cells get trapped in spleen Terminal blast phase “Blast crisis” Survival: Only 3 to 6 months

Question 229

Tx of CML

Answer 229

Chlorambucil (chemotherapeutic), administered with or without corticosteroids, on a daily or intermittent schedule Chemotherapy No cure for CML Tyrosine Kinase Inhibitors (e.g. Imatinib (Gleevec)) Combined chemotherapy Biologic response modifiers Allogeneic stem cell transplantation-from different genetic lines, not from direct close relative

Question 230

Lympadenophathy

Answer 230

enlarged lymph nodes that become palpable and tender

Question 231

Local lymphadenopathy

Answer 231

Drainage of an inflammatory lesion located near the enlarged node

Question 232

General Lymphadenopathy

Answer 232

Occurs in the presence of malignant or nonmalignant disease

Question 233

Causes of Lympadenopathy

Answer 233

Neoplastic disease Immunologic or inflammatory conditions Endocrine disorders Lipid storage diseases Unknown causes

Question 234

Primary lymphoid tissue

Answer 234

Thymus Bone marrow

Question 235

Secondary Lymphoid Tissue

Answer 235

SLIT Spleen Lymph nodes Intestinal Lymphoid tissue Tonsils

Question 236

2 categories of malignant lymphomas

Answer 236

-Hodgkin Lymphoma--linked to EBV -non-hodgkin lymphoma

Question 237

What is necessary for the diagnosis of Hodgkin lymphoma but not specific to Hodgkin Lymphoma?

Answer 237

Reed-Sternberg cells in lymph nodes

Question 238

What are Reed Sternberg cells derived from?

Answer 238

Are derived from malignant B cells that usually become binucleate. Release cytokines-signaling substances that signal other immune system cells to proliferate

Question 239

Clinical manifestations of Hodgkins lymphoma

Answer 239

Enlarged painless neck lymph nodes Lymphadenopathy, causing pressure or obstruction Mediastinal mass Fever, weight loss, night sweats, pruritus, fatigue

Question 240

Tests for Hodgkin's Lymphoma

Answer 240

Chest x-rays, lymphangiography, and biopsy (biopsy most indicative of Hodgkin lymphoma)

Question 241

Tx of Hodgkin's lymphoma

Answer 241

Approximate cure rate: 75% Combined treatment with radiation therapy and chemotherapy High-dose chemotherapy with bone marrow or stem cell transplantation Monoclonal antibodies Nonmyeloablative allogeneic stem cell transplantation

Question 242

Clinical manifestations of Non-hodgkin lymphoma

Answer 242

Localized or generalized painless lymphadenopathy Nodal enlargement and transformation over months or years Retroperitoneal and abdominal masses with symptoms of abdominal fullness and back pain Ascites (fluid in the peritoneal cavity) and leg swellin

Question 243

Treatment of non-hodgkin Lymphoma

Answer 243

Survival: Extended periods but less than the survival rate for Hodgkin lymphoma Dependent on the type (B cell or T cell), tumor stage, histologic status (low, intermediate, high grade), symptoms, age, and any co-morbidities Chemotherapy or radiation Combination of chemotherapy and radiation Monoclonal antibody: Rituximab Radioimmunotherapy: Combination of radiation therapy with monoclonal antibody therapy

Question 244

Burkitt Lymphoma

Answer 244

Highly aggressive B-cell non-Hodgkin lymphoma Very fast-growing tumor of the jaw and facial bones (Africa); rare in the United States EBV in 90% of cases Abdominal swelling for people affected in the United States Biopsy or bone marrow findings Treatment Radiotherapy and cyclophosphamide Adjuvant monoclonal antibody therapy with rituximab

Question 245

Lymphoblastic Lymphoma

Answer 245

Is a relatively rare variant of non-Hodgkin lymphoma (2% to 4%). Accounts for almost one third of cases in children and adolescents with a male predominance. More than 85% have T-cell origins. Clones of relatively immature T-cells become malignant in the thymus.

Question 246

First sign of lymphoblastic lymphoma

Answer 246

Painless lymphadenopathy in the neck.

Question 247

treatment of lymphoblastic lymphoma

Answer 247

Treatment: Combined chemotherapy with multiple drugs.

Question 248

Conditions that mimic lymphomas

Answer 248

Tuberculosis (TB) syphilis systemic lupus erythematosus lung cancer bone cancer Important distinction

Question 249

Plasma cell malignancies

Answer 249

multiple myeloma waldenstrom macroglobulinemia

Question 250

Clinical manifestations of multiple myeloma

Answer 250

Hypercalcemia, renal failure Anemia Lytic lesions (round, “punched out” regions of bone) Skeletal pain Hyperviscosity syndrome Recurring infections due to loss of the humoral immune response

Question 251

Tx of Multiple myeloma

Answer 251

Prognosis poor Combinations of chemotherapy, radiation therapy, and plasmapheresis (exchange) and bone marrow transplantation High-dose chemotherapy, followed by blood-forming stem cell transplantation Tandem transplant, or thalidomide, or both (are showing promise) Bisphosphonates: To reduce skeletal damage Hydration and diuretics: To maintain a high urine output Antibiotics: To treat recurring infections

Question 252

What is monoclonal gammopathy of undetermined significance

Answer 252

Occurs before multiple myeloma. Is diagnosed by the presence of an M protein in the blood or urine without additional evidence of multiple myeloma. Considered nonpathologic and requires no treatment. Asymptomatic multiple myeloma: Is referred to as smoldering myeloma and indolent myeloma

Question 253

What is Waldenstrom Macroglobulinemia?

Answer 253

Is also called lymphoplasmacytic lymphoma. Is a rare type of slow-growing plasma cell tumor that secretes a monoclonal immunoglobulin M (IgM) molecule. Arises from plasma cells that have genetic rearrangement of region genes (V, D, J).

Question 254

Manifestations of Waldenstrom Macroglobulinemia?

Answer 254

Weakness and fatigue bleeding (from gums and nose) weight loss bruising

Question 255

Treatment of Waldenstrom macroglobulinemia

Answer 255

Combined chemotherapy with nucleoside analogs, alkylating agents, and monoclonal antibody (e.g., rituximab).

Question 256

Thombocytopenia

Answer 256

Platelet count <100,000/mm3

Question 257

Platelets <50,000/mm3:

Answer 257

hemorrhage from minor trauma

Question 258

Platelet count <15,000/mm3:

Answer 258

spontaneous bleeding

Question 259

Platelet count <10,000/mm3:

Answer 259

severe bleeding that can be fatal

Question 260

Immune Thrombocytopenic Purpura (ITP)

Answer 260

IgG antibody targets platelet glycoproteins. Antibody-coated platelets are sequestered and removed from circulation. Acute form develops after viral infections. Is one of the most common childhood bleeding disorders. Chronic form usually is found in adults.

Question 261

Clinical manifestations of ITP

Answer 261

Petechiae and purpura, progressing to major hemorrhage

Question 262

Treatment of ITP

Answer 262

Palliative, not curative Prednisone Romiplostim (Nplate), Eltrombopag (Promacta) Both stimulate thrombopoietin to increase thrombocytes Splenectomy If unsuccessful, immunosuppressive drugs are used

Question 263

Thrombotic Thrombocytopenic purpura (TTP)

Answer 263

A thrombotic microangiopathy Platelets aggregate and cause occlusion of arterioles and capillaries.

Question 264

TTP Pathognomonic Pentad

Answer 264

Extreme thrombocytopenia Intravascular hemolytic anemia Ischemic signs and symptoms most often involving the CNS (approximately 65% exhibit memory disturbances, behavioral irregularities, headaches, or coma) Kidney failure Fever

Question 265

Treatment of TTP

Answer 265

Untreated acute TTP: Mortality rate of 90% Prompt treatment of acute TTP: Mortality rate reduced to 10% to 20% Plasma exchange with fresh frozen plasma Steroids Splenectomy: Performed if no response to treatment Immunosuppressive therapy: Azathioprine (Imuran)

Question 266

Thrombocythemia

Answer 266

Also called thrombocytosis Platelet counts: >400,000/mm3 Cause: Accelerated platelet production in the bone marrow Types: Primary or secondary (reactive) Causes intravascular clot formation (thrombosis), hemorrhage, or other abnormalities

Question 267

Essential (primary) thrombocythemia (ET)

Answer 267

Chronic myeloproliferative disorder Characterized by excessive platelet production, resulting from a defect in megakaryocyte progenitor cells Rare hereditary type of ET: Familial essential thrombocythemia (FET)

Question 268

Clinical manifestations of Essential thrombocythemia

Answer 268

Chronic myeloproliferative disorder Characterized by excessive platelet production, resulting from a defect in megakaryocyte progenitor cells Rare hereditary type of ET: Familial essential thrombocythemia (FET)

Question 269

Clinical manifestations of ET

Answer 269

Microvascular thrombosis, erythromyalgia, possible bleeding

Question 270

treatment of ET

Answer 270

Interferon, anagrelide (Agrylin), aspirin; prevent clots or bleeding

Question 271

Prolonged bleeding can result from alterations in platelet function:

Answer 271

Adhesion between platelets and the vessel wall Platelet-platelet adhesion Platelet granule secretion Arachidonic acid pathway activity Membrane phospholipid regulation

Question 272

Vitamin K deficiency

Answer 272

Necessary for synthesis and regulation of prothrombin, procoagulant factors (VII, IX, X), and proteins C and S (anticoagulants) Deficiency: Leads to bleeding Treatment: Parenteral administration of vitamin K

Question 273

Virchow Triad

Answer 273

Injury to the blood vessel endothelium: Atherosclerosis, many others Abnormalities of blood flow Hypercoagulability of the blood

Question 274

Antiphospholipid snydrome

Answer 274

Autoimmune syndrome characterized by autoantibodies against plasma membrane phospholipids and phospholipid-binding proteins Treatment: Heparin with aspirin

Question 275

Deficiencies in Protein S and S and AT III contribute to a ________________ state.

Answer 275

hypercoagulable

Question 276

Advantages of using specific components instead of whole blood

Answer 276

1. replacement of only the needed component 2. minimizing the risk of circulatory volume overload 3. minimizing the risk of allergic reactions to antibodies or antigens in donor plasma

Question 277

When is whole blood recommended?

Answer 277

in cases of severe hemorrhage to increase volume and oxygen carrying capacity

Question 278

Whole blood can be converted into specific components

Answer 278

-packed erythrocytes -platelet concentrates -Fresh frozen plasma -dried plasma (FDA approved for EUA for military use) -cryoprecipitated antihemophiliac factor -Factor IX concentrate -Fibrin Glue -Granulocyte concentrates -Albumin -Plasma protein fraction -immune globulin

Question 279

How are packed erythrocytes prepared?

Answer 279

by removing most of the plasma from whole blood

Question 280

How much of whole blood is packed erythrocytes?

Answer 280

30%

Question 281

Advantage of packed erythrocytes

Answer 281

-lower sodium, potassium, ammonia, citrate, and lactate than whole blood, so useful in patients with renal or hepatic impairment

Question 282

Shelf life of erythrocytes can be extended up to______ days in certain buffer/preservative solutions

Answer 282

49

Question 283

Can packed erythrocytes be frozen?

Answer 283

yes, can be frozen in glycerol (antifreez) for up to 3 years. Cells must be washed of glycerol prior to use -frozen storage is expensive so is only appropriate for rarest blood types

Question 284

Primary use of packed erythrocytes

Answer 284

to increase oxygen carrying capacity in non-hypovolemic states

Question 285

Packed erythrocytes administered with hypotonic diluents can cause:

Answer 285

osmotic lysis

Question 286

What are platelets prepared from?

Answer 286

Whole blood

Question 287

How many platelets/unit?

Answer 287

5-10 million

Question 288

How are platelets stored?

Answer 288

at room temp since refrigeration tends to decrease platelet aggregation ability -bacterial growth at room temp is a problem so storage limited to 5 days

Question 289

normal thrombocytopenia use requires an average of ________ platelets.

Answer 289

40 million platelets (appro equivalent to 6 units of blood)

Question 290

True/false: due to large numbers of leukocytes in concentrate, patients should be given platelets from matching blood group donors (including Rh factors)

Answer 290

true

Question 291

How is fresh frozen plasma prepared?

Answer 291

from whole blood by separating from RBCs and platelets

Question 292

Which coagulant factors are present in FFP?

Answer 292

except for platelets, all other procoagulant factors are present

Question 293

Can FFP be frozen?

Answer 293

yes, can be kept up to 12 months in frozen state, once thawed must be used within a few hours

Question 294

How much FFP can be obtained from a unit of whole blood?

Answer 294

250mL

Question 295

Which electrolyte is high in FFP?

Answer 295

sodium load is high

Question 296

IS matching blood donor of FFP required?

Answer 296

use from matching blood donors prefered but not mandatory Allergic reactions possible

Question 297

What is FFP used for?

Answer 297

to treat active bleeding in patients with low coagulation factors -used in cases of warfarin overdose or surgery in patients taking warfarin -use in treating hypovolemia not recommended

Question 298

Which blood factor is Cryoprecipitated antihemophiliac factor?

Answer 298

blood factor VIII

Question 299

What is cryoprecipitate??

Answer 299

precipitated forms when FFP is thawed

Question 300

How soon should cryo be used after thawing

Answer 300

within 3 hours

Question 301

What does Cryoprecipitated contain large amounts of?

Answer 301

fibrinogen fibrinogenemia is possible with multiple dosing

Question 302

_____________is resuspended in 9-16ml plasma and stored frozen for up to 1 year.

Answer 302

cryoprecipitate

Question 303

What is a possibility when cryo is used in patients with type A, B, or AB blood groups?

Answer 303

hemolytic anemia, so use matching type form or type O if hemolytic anemia seen

Question 304

Primary use of cryoprecipitate?

Answer 304

treatment of patients with hemophilia A also given prophylactically prior to surgery or giving birth in patients with congenital fibrinogen deficiency or von willebrands disease that is unresponsive to desmopressin.

Question 305

Desmopressin is a synthetic ADH analog which increases factor ____ activity in hemophiliacs and von willebrand patients.

Answer 305

8

Question 306

What is Factor IX concentrate also known as?

Answer 306

prothrombin complex

Question 307

How is Factor IX concentrate prepared?

Answer 307

prepared from pooled plasma

Question 308

is there a need for blood typing prior to use of Factor IX?

Answer 308

no

Question 309

Risk of Factor IX concentrate

Answer 309

hepatitis and thrombosis, especially in patients with liver disease

Question 310

Factor IX is stable for _____ hrs after reconstitution

Answer 310

12 hours

Question 311

__________is not found in cryoprecipitated antihemophiliac factor.

Answer 311

Factor IX concentrate

Question 312

Fibrin Glue

Answer 312

-prepared from bovine thrombin and human fibrinogen, which clots when mixed. -used to seal bleeding suture holes -allergic reactions reported

Question 313

How do antifibrinolytics work? ex. TXA

Answer 313

form a reversible complex with plasminogen and plasmin thus blocking plasminogen from interacting with fibrin and blocking plasmin's proteolytic activity

Question 314

synthetic antifibrinolytics

Answer 314

aminocaproic acid Tranexamic acid

Question 315

Natural antifibrinolytics

Answer 315

aprotinin

Question 316

Granulocyte concentrates

Answer 316

-used to treat some infections in patients with low granulocyte concentrations -fever following administration is common and can be treated by giving antihistamines and antipyretics

Question 317

How is albumin obtained?

Answer 317

from human plasma fractions

Question 318

How long can albumin be stored?

Answer 318

for 3 yrs

Question 319

How is the risk of viral disease transmission reduced with albumin?

Answer 319

heating to 60 C for 10 hrs

Question 320

What is albumin used for?

Answer 320

to treat hypoalbuminemia by administering 25% solution (which is hypertonic and causes increased plasma volume by pulling interstitial fluid into vascular system)

Question 321

Plasma protein fraction contains at least _____% albumin and no more than _____% globulins in saline

Answer 321

83% albumin 17% globumin 5% protein solution

Question 322

What is equivalent osmotically to plasma?

Answer 322

plasma protein faction

Question 323

what is plasma protein fraction used for ?

Answer 323

to treat hypovolemic shock and hypoproteinemia

Question 324

Immunoglobulin

Answer 324

concentrated solution of globulins (mainly immunogobulins) prepared from human plasma -used to modify infection progression of several dz (hep A, rubella, varicella)

Question 325

Where is heparin found?

Answer 325

mast cell and nerve terminal vesicles

Question 326

Structurally heparin is a ________.

Answer 326

glycosaminoglycan

Question 327

What does heparin require for action?

Answer 327

co-factor--Antithrombin III

Question 328

What does the heparin complex inhibit?

Answer 328

coagulation factors IXa, Xa, XIA, XIIa and thrombin activity

Question 329

How is heparin eliminated and metabolized?

Answer 329

50% metabolized and 50% eliminated unchanged in the urine with a t1/2 of 1-2 hours t1/2 increases dramatically in liver or renal disease

Question 330

Topical hemostatics

Answer 330

Substances include: -absorbable gelatin sponge (Gelfoam) -absorbable gelatin film (Gelfilm) -oxidized cellulose (oxycel) -microfibrillar collagen hemostat (avitene) -thrmobin powder

Question 331

Blood substitutes

Answer 331

-oxygen-carrying volume expanders -longer shelf-life than most blood products -no risk of disease transmission or blood-group reactions -useful in instances of inadequate blood supplies -do not have coagulation factors, so not much use in bleeding patients -1/2 lives short so use limited to emergency hypovolemia or shock -can cause nephrotoxicity, HTN and diminished coag component concentrations

Question 332

Blood substitute agents include:

Answer 332

-Hydroxyethyl starch -dextrans -perfluorocarbons -hemoglobin-based substitutes

Question 333

Hydroxyethyl starch

Answer 333

-complex polysaccharide -available in 6% solution for volume expansion -fairly long half-life (similar to albumin solutions)

Question 334

Side effects of Hydroxyethyl starch

Answer 334

-increased serum amylase concentrations and pruruitis may also cause prolongation of thromboplastin time and decreased factor VII, fibrinogen and von willebrand factor which results in decreased platelet adhesion and decreased clot strength

Question 335

Dextran ______ is a water-soluble glucose polymer.

Answer 335

70

Question 336

How is dextran 40 formed?

Answer 336

from dextran 70

Question 337

Dextran-40 is removed in _______ and Dextran-70 is converted enzymatically to ________

Answer 337

glomerulus glucose

Question 338

How long do dextrans remain in plasma for?

Answer 338

12 hours

Question 339

What are dextrans used for ?

Answer 339

plasma fluid volume expansion

Question 340

Side effects of dextrans

Answer 340

-allergic rxn (dextran 40<70) -increased bleeding times due to decreased platelet adhesion

Question 341

What are perfluorocarbons (Fluosol-DA 20)

Answer 341

sythetic compounds that act like HGB by binding large amounts of oxygen -small size travel through narrowed vessels -removed from market in 1994 but research continues on similar compounds (ie oxygen)

Question 342

Problems with use include:

Answer 342

-short shelf life -temperature instability -short 1/2 life -side effects including disruption of pulmonary surfactant mechanisms, allergic reactions

Question 343

Hemoglobin based

Answer 343

-effective at carrying oxygen to tissues -purified Hb cannot be given directly as it caused renal toxicity -required very specific coatings/encapsulation to avoid toxicity and carry oxygen -several products in development and clinical trials -military especially interesting -currently testing "dried blood" for reconstitution

Question 344

Erythropoiesis begins in the vessels of the _______.

Answer 344

yolk sac

Question 345

After ______ weeks gestation, the erythrocytes deliver oxygen.

Answer 345

2

Question 346

At _____ weeks gestation, erythrocyte production shifts to the liver sinusoids (peaks at 4 months).

Answer 346

8

Question 347

By ______months gestation, erythrocyte production beings in the bone marrow.

Answer 347

5

Question 348

At delivery, _________ is the only significant hematopoiesis site.

Answer 348

marrow

Question 349

Btwn ______ and ______ months of age: normal adult hgb percentages are established.

Answer 349

6-12 months

Question 350

Embryonic hemoglobins

Answer 350

Gower 1 Gower 2 Portland

Question 351

Fetal hemoglobin has how many alpha and gamma chains

Answer 351

2 alpha chains and 2 gamma chains

Question 352

Full term normal erythrocyte lifespan is ________ days.

Answer 352

60-80 days have many reticulocytes

Question 353

Premature infants erythrocyte lifespan is __________.

Answer 353

20-30 days

Question 354

Children and adolescents erythrocyte lifespan =________________days.

Answer 354

120 days

Question 355

When does hemotopoiesis increase

Answer 355

-during fetal life -trauma of birth -cutting of umbilical cord

Question 356

What are all high at birth but start to decline to adult levels.

Answer 356

Neutrophils eosinophils monocytes

Question 357

Platelet counts in full-term neonates

Answer 357

comparable to platelet counts in adults and tend to remain so through infancy and childhood

Question 358

Lymphocyte levels at birth

Answer 358

high at birth and continue to rise in some healthy infants during the first year of life then a steady decline occurs throughout childhood and adolescence until adult values reached

Question 359

What is the most common blood disorder in children?

Answer 359

anemia

Question 360

Causes of anemia in children

Answer 360

-ineffective erythropoiesis -premature destruction of erythrocytes -most common cause: iron deficiency

Question 361

Hemolytic anemias

Answer 361

-premature destruction caused by intrinsic abnormalities of erythrocytes -damaging extraerythrocytic factors -inherited, congenital or both

Question 362

Iron deficiency anemia

Answer 362

-most common blood disorder of infancy and childhood -stored iron: greatest stores are present 4--8 weeks after birth -dietary iron-needed after 16-20 weeks of age -lack of iron intake or blood loss

Question 363

clinical manifestations of iron-deficiency anemia in children

Answer 363

-irritability -decreased activity tolerance -tachycardia -weakness -lack of interest in play -pica -may affect attention span, alertness and learning

Question 364

treatment of iron deficiency anemia in children

Answer 364

iron with vitamin C cow's milk restricted

Question 365

What is hemolytic disease of the newborn (HDN)

Answer 365

-also: erythroblastosis fetalis -as hemolysis progresses the fetus becomes anemic, as a result, erythropoiesis and immature nucleated cells (erythroblasts) are released into the blood stream -maternal blood and fetal blood are antigenically incompatible -maternal antibody is directed against fetal antigents -between 20-25% ABO incompatible; less than 10% are Rh incompatible but is more severe

Question 366

what is an alloimmune disease?

Answer 366

hemolytic disease of the newborn/erythroblastosis fetalis

Question 367

Clinical manifestations of HDN

Answer 367

-anemia -hyperbilirubinemia -icterus neonatorum (neonatal jaundice) kernicterus: bilirubin deposited in the brain and can cause death

Question 368

Test for HDN

Answer 368

Coombs

Question 369

Treatment of HDN

Answer 369

-prevention: Rh immune globulin (rhoGam) -if not treated, phototherapy, exchange transfusion

Question 370

Glucose-6-phosphate dehydrogenase deficiency

Answer 370

-inherited x-linked, recessive disorder -G6PD: enzyme helps erythrocytes maintain metabolic processes, despite injurious conditions -deficiency shortens RBC lifespan

Question 371

s/s of G6PD

Answer 371

asymptomatic unless stressor are present -icterus neonatorum -acute hemolytic anemia-pallor, icterus, dark urine, back pain -between hemlytic episodes: no anemia; erythrocyte survival is normal

Question 372

What happens without G6PD?

Answer 372

oxidative stressors damage hgb and the plasma membranes of erythrocytes (Heinz bodies-denatured hgb particles in erythrocytes)

Question 373

Treatment of G6PD

Answer 373

preventon: high-risk group tested for hemolysis: blood transfusions and oral iron therapy spontaneous recovery: generally follows tx

Question 374

What is hereditary spherocytosis also called?

Answer 374

-congenital hemolytic anemia -congenital acholuric jaundice

Question 375

What is hereditary spherocytosis?

Answer 375

-autosomal dominant trait -most common of hemolytic disorders in which no hgb abnormality exists -abn of proteins or spectrins of the erythrocyte membrane leading to an increased concentration of intracellular sodium

Question 376

Clinical manifestations of hereditary spherocytosis

Answer 376

anemia jaundice splenomegaly

Question 377

treatment of hereditary spherocytosis

Answer 377

-daily folic acid supplementation to increase the production of healthy RBC -may need partial splenectomy

Question 378

Sickle cell disease

Answer 378

-characterized by the precence of an abnormal hemoglobin (Hb S) -autosomal recessive -mutation causes valine to be replaced by glutamic acid -deoxygenation and dehydration: RBC solidify and stretch into an elongated sickle shape -sickle cell trait: child inherits Hb S from one parent and normal Hb A from other; heterozygous carrier rarely has symptoms

Question 379

Polymerization

Answer 379

sickled erythrocyte stiffens, changing from a flexible beneficial cell to an inflexible one that starves and damages tissues

Question 380

Aplastic crisis

Answer 380

transient cessation in RBC production occurs as a result of viral infection

Question 381

Sequestration crisis

Answer 381

large amounts of blood pool in the liver and spleen

Question 382

hyperhemolytic crisis

Answer 382

rate of RBC destruction is accelerated

Question 383

Acute chest syndrome

Answer 383

sickled RBC attach to the endothelium of the injured, underventilated and inflamed lung and fail to be reoxygenated

Question 384

Sickle Cell Hb C disease

Answer 384

usually milder than sickle cell anemia

Question 385

Clinical manifestation of sickle cell disease

Answer 385

infection: most common cause of death -glomerular disease-the inability of the tubules of the kidneys to concentrate urine, bed wetting, proteinuria -gallstones or cholecystitis

Question 386

Treatment of sickle cell disease

Answer 386

prevention of crises: avoid fever, infection, acidosis, dehydration, constricting clothes, exposure to cold -immediate correction of acidosis and dehydration with appropriate IVF -routine childhood immunizations -infections: aggressive abx -oxygen: not needed unless individual is hypoxic -management of pain -genetic counseling and psychologic support

Question 387

Thalassemias

Answer 387

-autosomal recessive disorders -slowed or defective synthesis of globin chains of hgb molecule: alpha or beta -major: homozygous inheritance -minor: heterozygous inheritance

Question 388

alpha thalassemia

Answer 388

alpha chains affected

Question 389

Beta thalassemia

Answer 389

beta chains affected

Question 390

Beta-thalassemia major

Answer 390

cooley anemia can be fatal

Question 391

Alpha-thalassemia minor

Answer 391

2 genes

Question 392

Alpha thalassemia major

Answer 392

4 genes; fatal

Question 393

hemoglobin H disease

Answer 393

3 genes

Question 394

Beta thalassemia minor

Answer 394

mild- to moderate hypochromic microcytic anemia, mild splenomegaly bronze coloring of skin hyperplasia of bone marrow usually asymptomatic

Question 395

Beta thalassemia major

Answer 395

severe anemia resulting in large CV burden

Question 396

Alpha trait s/s

Answer 396

symptom free having mild microcytosis at most

Question 397

s/s alpha thalassemia minor

Answer 397

virtually idential to those of beta thalassemia minor

Question 398

alpha thalassemia major

Answer 398

hydrops fetalis-edema of fetus or infant involving multiple compartments -fulminant intrauterine congestive heart failure-fetus has a grossly enlarged heart and liver -dx usually made post mortem

Question 399

treatment for thalassemia major

Answer 399

-genetic counseling -blood transfusions -iron chelation therapy -splenectomy -bone marrow, cord blood and stem cell transplantation-currently only cure

Question 400

Hemophilia A

Answer 400

-classic hemophilia -factor VIII deficiency -X-linked

Question 401

Hemophilia B

Answer 401

-christmas disease -factor IX deficiency

Question 402

Hemophilia C

Answer 402

Factor XI deficiency

Question 403

von Willebrand disease:

Answer 403

autosomal dominant trait of factor VIII deficiency

Question 404

two primary defects of hemophilias

Answer 404

point mutation gene deletion

Question 405

Clinical manifestations of hemophilias

Answer 405

-hematoma formations -persistent bleeding from relatively minor traumatic lacerations

Question 406

Tests of hemophilias

Answer 406

Phase III: thrombin time Phase II: prothrombin time Phase i: activated partial thromboplastin time, prothrombin consumption time, thromboplastin generation test (most sensitive)

Question 407

Treatment of hemophilias

Answer 407

-recombinant factor VIII -recombinant antihemolytic factor plasma; albumin free method: for hemophilia A

Question 408

Congenital hypercoagulability and thrombosis

Answer 408

-thrombophilia -defecting in clotting factors -protein C deficiency -neonatal purpura fulminans: fatal -protein S deficiency -antithrombin III (ATIII) deficiency

Question 409

treatment of congenital hypercoagulability and thrombosis

Answer 409

anticoagulants, especially heparin and recplacement of deficient factor

Question 410

idiopathic thrombocytopenic purpura

Answer 410

-autoimmune or primary thrombocytopenic purpura -antiplatelet antibodies bind to platelet plasma membranes, causing platelet sequestration and destruction -occurs after a viral infection

Question 411

Clinical manifestations of idiopathic thrombocytopenic purpura

Answer 411

-bruising -gen petechial rash -asymmetrical bleeding

Question 412

treatment of ITP

Answer 412

fresh blood or platelet transfusion and corticosteroids -75% completely recover within 3 months, even without tx

Question 413

Autoimmune neonatal thrombocytopenia

Answer 413

-immunologic destruction of platelets by antibodies (IgG)

Question 414

Autoimmune neonatal thrombocytopenia purpura

Answer 414

maternal immunization against fetal paternally derived platelet specific antigens

Question 415

Autoimmune vascular purpura

Answer 415

-allergic purpura -antibody mediated injury of blood vessel walls, typically arterioles and capillaries

Question 416

Leukemia

Answer 416

-most common malignancy of childhood -acute lymphocytic leukemia (ALL) 75-80% of all leukemias in children -unclear cuase-genetic susceptibility, environmental factors, viral infections

Question 417

Clinical manifestations of leukemia

Answer 417

-pallor -fatigue -petechiae -purpura -bleeding -fever( hypermetabolism and infections) -bone pain

Question 418

Treatment of leukemia

Answer 418

-combo chemo -radiation -induction of remission; preventitive therapy for CNS; intensification (consolidation) ; mainenance

Question 419

Non-hodgkin lymphoma

Answer 419

-implicated factors: defective host immunity, viral agent, chronic immunostimulation and genetic predisposition -nodular and diffuse -abdomen or chest -tx: chemo -prognosis: favorable with a 70-80% cure rate

Question 420

hydroureter

Answer 420

dilation of the ureters

Question 421

hydronephrosis

Answer 421

dilation of the renal pelvis and calyces

Question 422

ureterohydronephrosis

Answer 422

dilation of both the ureters and renal pelvis and calyces

Question 423

tubulointerstitial fibrosis

Answer 423

deposition of excessive amounts of extracellular matrix

Question 424

What is post obstructive diuresis caused by?

Answer 424

relief of the obstruction -may cause fluid and electrolyte imbalance

Question 425

Risk factors for kidney stones

Answer 425

-male -most develop before 50 years of age -inadequate fluid intake: most prevalent -geographic location: temperature, humidity, rain fall, fluid, and dietary patterns

Question 426

composition of kidney stones

Answer 426

composition of mineral salts -calcium oxalate and calcium phosphate: 70-80% -struvite (magnesium, ammonium, phosphate): 15% -uric acid: 7%

Question 427

Staghorn calculi

Answer 427

-large and fill the minor and major calyces

Question 428

Genetic disorders of amino acid metabolism

Answer 428

excess in urine can cause cystinuric and xanthine, stone formation in the presence of low urine pH

Question 429

Kidney stone formation

Answer 429

supersaturation of one or more salts -presence of a salt in a higher concentration than the volume is able to dissolve in the salt precipitation of a salt form a liquid to a solid state -temperature and pH growth into a stone via crystallization or aggregation -process by which crystals grow from a small nidus or nucleus to larger stones -embedded in the matrix

Question 430

What increases the risk of calcium phosphate stone formation?

Answer 430

alkaline urinary ph

Question 431

What increases the risk of a uric acid stone?

Answer 431

acidic urine

Question 432

What prevents stone formation?

Answer 432

-potassium citrate -pyrophosphate -magnesium calcium and phosphate and oxalate types

Question 433

Clinical manifestation of kidney stones

Answer 433

renal colic (pain)

Question 434

treatment of kidney stones

Answer 434

-parental and/or analgesics for acute pain -medical therapy that promotes stone passage (alpha--antagonists or calcium channel blockers) -high fluid intake -alteration in urine pH -removal of stones using percutaneous nephrolithotomy, uteroscopy, or ultrasonic or laser lithotripsy to fragment stones for excretion

Question 435

Neurogenic bladder

Answer 435

bladder dysfunction caused by neurologic disorders that interrupt innervation

Question 436

Neurogenic bladder affecting upper motor neurons

Answer 436

-dyssynergia: overactive or hyperreflexive bladder function -detrusor hyperreflexia: uninhibited or reflex bladder -detrusor hyperreflexia with vesicosphincter (detrusor sphinctor) dyssynergia: both the bladder and sphincter are contracting at the same time, causing a functional obstruction of the bladder outlet

Question 437

Neurogenic bladder affecting lower motor neurons

Answer 437

detrusor areflexia: underactive, hypotonic, or atonic bladder

Question 438

Causes of lower urinary tract obstruction

Answer 438

-prostate enlargement -urethral stricture -severe pelvic organ prolapse -low bladder wall compliance

Question 439

clinical manifestations of lower urinary tract obstruction

Answer 439

-frequent daytime voiding: more often than every 2 hours while awake -nocturia: night-time voiding -urgency: often combined with hesitancy -dysuria -poor force of stream; intermittency of urinary stream -feelings of incomplete bladder emptying despite micturition

Question 440

if determining poor detrusor contraction strength versus obstruction the following are needed:

Answer 440

-multichannel urodynamic testing -video-urodynamic recordings -functional imaging studies and serum creatinine -electromyography

Question 441

treatment of lower urinary tract obstruction

Answer 441

-detrusor sphincter dyssynergia -alpha adrenergic blocking and/or antimuscarinic medications or botulinum toxin - intermittent catheterization in combo with higher dose antimuscarinic drugs -condom catheter containment, supplemented by an alpha adrenergic blocking drug or transurethral sphincterotomy (surgical incision of the striated sphincter) -obstruction -medication -bladder neck incision

Question 442

treatment of prostate enlargement

Answer 442

-caused by acute inflammation, benign prostatic hyperplasia, or prostate cancer -medication (flomax) -surgery

Question 443

treatment of low bladder wall compliance

Answer 443

-antimuscarinic drugs and intermittent catheterization -severe cases: augmentation enterocystoplasty (englargement of bladder wall causing detubularized piece of small bowel), urinary diversion or long-term indwelling catheterization

Question 444

tx of urethral stricture

Answer 444

urethral dilation with a steel instrument shaped similar to a catheter (urethral sound) or a series of incrementally increasing catheter like tubes (filiforms and followers) -long, dense strictures, typically requiring surgical urethroplasty

Question 445

Tx of prolapse

Answer 445

pressary: rubber or silicone device designed to compensate for vaginal wall prolapse -intravaginally hormone replacement therapy and regular follow-up -sx

Question 446

Overactive bladder syndrome

Answer 446

-chronic syndrome of detrusor overactivity -symptom syndrome of urgency, with or without urge incontinence; usually associated with frequency and nocturia

Question 447

treatment of overactive bladder syndrome

Answer 447

-lifestyle modifications -behavioral modifications -pharmacotherapy (antimuscarinic agents, botulinum toxin)

Question 448

Are renal adenomas benign?

Answer 448

yes

Question 449

most common renal tumor

Answer 449

renal cell carcinoma

Question 450

What is caused by mutrations of the von-Hippel Lindau gene located on chromosome 3p

Answer 450

renal cell carcinoma

Question 451

clinical manifestations of renal cell carcinoma

Answer 451

-hematuria -dull and aching flank pain

Question 452

tx of renal cell carcinoma

Answer 452

-localized: surgical removal of affected kidney (radical nephrectomy) or partial nephron sparing nephrectomy for smaller tumors -surgery, chemo, radiation

Question 453

most common bladder tumor

Answer 453

urothelial (transitional cell) carcinoma

Question 454

risk factors for urothelial (transitional cell) carcinoma

Answer 454

-smoking -exposure to metabolites of aniline dyes or other aromatic amines or chemicals -highly arsenic in drinking water -heavy consumption of phenacetin

Question 455

pyelonephritis

Answer 455

inflammation of upper urinary tract

Question 456

pyelonephritis

Answer 456

bladder inflammation

Question 457

Protective urinary mechanisms of UTI

Answer 457

-washed out of urethra during micturition -low pH and high osmalality of urine -presence of Tamm-Horsfall protein -secretions from the uroepithelium: bactericidal effect -uterovesical junction: closes to prevent reflux of urine to the ureters and kidneys -women: mucous secretion glands -men: length of male urethra -lewis blood group

Question 458

Most common pathogens of UTI

Answer 458

-escherichia coli -staphylococcus saprophyiticus

Question 459

Acute pyelonephritis

Answer 459

acute infection of the ureter, renal pelvis and/or renal parenchyma

Question 460

clinical manifestations of pyelonephritis

Answer 460

-flank pain -fever, chill; -costovertebral tenderness -purulent urine

Question 461

treatment of pyelonephritis

Answer 461

abx

Question 462

chronic pyelonephritis

Answer 462

-persistent or recurrent infections of the kidneys leading to scarring of the kidneys -inflammation and fibrosis, located in the intersitial spaces between tubules leading to chronic kidney failure. Tx : abx

Question 463

Glomerulopathies

Answer 463

disorders that directly affect the glomerulus -sig cause of chronic kidney disease and end stage renal failure worldwide

Question 464

Patho of acute glomerulonephritis

Answer 464

-formation of immune complexes (antigen/antibody) in the circulation with subsequent deposition in glomerulus -antibodies produced against the organism that cross-react with the glomerular endothelial cells -activation of complement -recruitment and activation of immune cell and mediators -decreased GFR as a result of inflammation glomerular sclerosis (scarring) -thickening of the glomerular basement membrane, but increased permeability of proteins and RBCs

Question 465

What is the most common form of acute glomerulonephritis?

Answer 465

Berger disease (immunoglobulin A, IgA) nephropathy

Question 466

Berger disease (IgA nephropathy)

Answer 466

-binding of abnormal IgA to mesangial cells in the glomerulus, resulting in injury and mesangial proliferation -autoimmune?

Question 467

Most common cause of Bergers disease

Answer 467

membraneous nephropathy -complement mediated gloumerular injury with increased glomerular permeability and glomerulosclerosis

Question 468

crescentic glomerulonephritis

Answer 468

-rapidly progressive -injury that results in the proliferation of glomerular capillary endothelial cells with rapid loss of renal function

Question 469

mesangial proliferative glomerulonephritis

Answer 469

immune complex in the mesangium with mesangial cell proliferation

Question 470

membranoproliferative glomerulonephritis

Answer 470

involves mesangial cell proliferation, complement deposition and crescent formation

Question 471

Clinical manifestations of acute glomerulonephritis

Answer 471

-hematuria with RBC -smoky, brown-tinged urine -proteinuria exceeding 2-5g/day with albumin -low serum albumin -edema -severe or progressive glomerular disease: eventual oliguria oliguria: UOP <30ml/hr or <400ml/day

Question 472

nephrotic sediment clinical manifestations

Answer 472

Contains massive amounts of protein and lipids and either a microscopic amount of blood or no blood.

Question 474

Nephritic sediment clinical manifestations

Answer 474

Blood is present in the urine with red cell casts, white cell casts, and varying degrees of protein, which is not usually severe.

Question 475

tx of acute glomerulonephritis

Answer 475

Antibiotics Corticosteroids Cytotoxic agents Anticoagulants

Question 476

Diabetic nephropathy

Answer 476

Podocyte injury, progressive thickening and fibrosis of the glomerular basement membrane, and expansion of the mesangial matrix

Question 477

lupus nephritis

Answer 477

Inflammatory complication of the chronic autoimmune syndrome, systemic lupus erythematosus Formation of autoantibodies against double-stranded deoxyribonucleic acid (DNA) and nucleosomes with glomerular deposition of the immune complexes

Question 478

chronic glomerulonephritis

Answer 478

-glomerular diseases with a progressive course, leading to chronic kidney failure -Diabetic nephropathy -lupus nephritis

Question 479

Clinical manifestations of chronic glomerulonephritis

Answer 479

-proteinuria -hypercholesterolemia

Question 480

treatment of chronic glomerulonepritis

Answer 480

-dialysis transplantation

Question 481

nephrotic syndrome

Answer 481

Excretion of 3.0g or more of protein in urine protein excretion as a result of glomerular injury

Question 482

tx of nephrotic syndrome

Answer 482

Normal-protein (1 g/kg body weight/day) and low-fat diet, salt restriction, diuretics, immunosuppression, and heparinoids Immunosuppressive drugs and angiotensin-converting enzyme inhibitors used when steroid-resistant

Question 483

Nephritic syndrome

Answer 483

Hematuria (usually microscopic) and red blood cell casts are present in the urine in addition to proteinuria, which is not severe.

Question 484

Advanced stages of nephritic syndrome

Answer 484

-HTN -uremia -oliguria

Question 485

cause of nephritic syndrome

Answer 485

Caused by increased permeability of the glomerular filtration membrane Pore sizes enlarge. Red blood cells and protein pass through.

Question 486

Renal insufficiency

Answer 486

decline of renal function to approx 25% of normal

Question 487

renal failure

Answer 487

significant loss of renal function (less than 15% of normal function)

Question 488

end stage renal failure

Answer 488

less than 10% of renal function remains

Question 489

uremia

Answer 489

Syndrome of renal failure Elevated blood urea and creatinine levels Fatigue, anorexia, nausea, vomiting, pruritus, and neurologic changes Retention of toxic wastes, deficiency states, electrolyte disorders, and proinflammatory state

Question 490

Azotemia

Answer 490

Increased serum urea levels and frequently increased creatinine levels Renal insufficiency or renal failure, causing azotemia Both azotemia and uremia: Accumulation of nitrogenous waste products in the blood

Question 491

Acute kidney injury

Answer 491

Sudden decline in kidney function with a decrease in glomerular filtration and accumulation of nitrogenous waste products in the blood Increase in serum creatinine and blood urea nitrogen

Question 492

classification of acute kidney injury

Answer 492

RIFLE: Risk; Injury; Failure; Loss; End-stage disease Criteria to guide the diagnosis of renal injury

Question 493

prerenal acute kidney injury

Answer 493

renal hypoperfusion most common cause

Question 494

infrarenal acute kidney injury

Answer 494

-disorders involving the renal parenchymal or interstitial tissue --acute tubular necrosis (ATN) caused by ischemia -most common cause

Question 495

post renal acute kidney injury

Answer 495

rare disorders associated with acute urinary tract obstruction

Question 496

Oliguria

Answer 496

Less than 400 ml of urine output per day Alterations in renal blood flow Efferent arteriolar vasoconstriction Impaired autoregulation

Question 497

oliguria processes-tubular obstruction

Answer 497

-necrosis of tubules causes sloughing of cells, cast formation or ischemia edema, which results in obstruction

Question 498

Backleak

Answer 498

-GFR remains normal, but tubular reabsorption or a "leak" of filtrate is accelerated from permeability

Question 499

initiation phase of AKI

Answer 499

Reduced perfusion or toxicity, during which renal injury is evolving. Usually lasts 24 to 36 hours. Prevention of injury is possible.

Question 500

Maintainance or oliguric phase of AKI

Answer 500

Period of established renal injury and dysfunction after the initiating event has been resolved. May last from weeks to months. Urine output is lowest, and serum creatinine, blood urea nitrogen, and serum potassium increase, metabolic acidosis develops, and salt and water overload occurs.

Question 501

Recovery phase of AKI

Answer 501

Renal injury is repaired, and normal renal function is reestablished. GFR returns toward normal, but the regenerating tubules cannot concentrate the filtrate. Diuresis is common, with a decline in serum creatinine and urea and an increase in creatinine clearance. Polyuria can result in excessive loss of sodium, potassium, and water.

Question 502

treatment of AKI

Answer 502

Correct fluid and electrolyte disturbances. Manage blood pressure. Prevent and treat infections. Maintain nutrition. Remember certain drugs can be toxic.

Question 503

tx of kyperkalemia

Answer 503

Hyperkalemia Restrict dietary sources of potassium. Use non–potassium-sparing diuretic agents, or use cation-ion exchange resins. Administer glucose and insulin or sodium bicarbonate to drive potassium into the cells. Administer calcium. May need dialysis.

Question 504

Tx of azotemia

Answer 504

-adopt a low-protein, high- carb diet

Question 505

chronic kidney disease

Answer 505

Progressive loss of renal function associated with systemic diseases Kidney damage: GFR less than 60 mL/min/1.73 m2 for 3 months or more, irrespective of cause Clinical manifestations: Do not occur until renal function declines to less than 25% of normal

Question 506

theory of CKD

Answer 506

Intact nephron hypothesis Loss of nephron mass with progressive kidney damage causes the surviving nephrons to sustain normal kidney function.

Question 507

Factors that advance CKD

Answer 507

Proteinuria Contributes to tubulointerstitial injury by promoting inflammation and progressive fibrosis. Angiotensin II Promotes glomerular hypertension, and participates in tubulointerstitial fibrosis and scarring.

Question 508

actors that contribute to progression of disease

Answer 508

Glomerular hypertension Hyperfiltration Tubulointerstitial inflammation Fibrosis

Question 509

Clinical manifestations of CKD

Answer 509

Affects every body system Uremic syndrome Proinflammatory state with the accumulation of urea and other nitrogenous compounds Toxins Alterations in fluid and electrolyte and acid-base balance

Question 510

Additional clinical manifestations of CKD

Answer 510

Calcium, phosphate, and bone Decreased calcium, causing renal osteodystrophies Hyperphosphatemia Acid-base balance Metabolic acidosis: Common Protein, carbohydrates, and fats metabolism Negative nitrogen balance, serum protein decreases Glucose intolerance High ratio of low-density lipoprotein (LDL) to high-density lipoprotein (HDL); high triglycerides increased serum creatinine and urea levels Cardiovascular system Cardiovascular disease: Major cause of morbidity and mortality; dyslipidemia Anemia: Lack of erythropoietin Hypertension: Volume overload Pulmonary system Dyspnea and Kussmaul respirations Hematologic alterations Normochromic normocytic anemia Impaired platelet function (bleeding) and hypercoagulability

Question 511

GI clinical manifestations of CKD

Answer 511

Gastrointestinal system Uremic gastroenteritis: Bleeding ulcer and significant blood loss Anorexia, nausea, vomiting, constipation, or diarrhea Uremic fetor: Bad breath caused by the breakdown of urea by salivary enzymes Malnutrition: Common

Question 512

Endocrine and reproductive S/S of CKD

Answer 512

Decrease in circulating sex steroids Decreased libido Insulin resistance Low thyroid hormone levels

Question 513

Integumentary system s/s of CKD

Answer 513

Anemia: Pallor Bleeding: Hematomas and ecchymosis Retained urochromes: Sallow skin color Hyperparathyroidism and uremic skin residues, known as uremic frost: Irritation and pruritus with scratching, excoriation, and increased risk for infection

Question 514

Tx of CKD

Answer 514

Management of protein intake Supplemental Vitamin D Maintenance of sodium and fluid Restriction of potassium Maintenance of adequate caloric intake Management of dyslipidemia Erythropoietin as needed ACE inhibitors or receptor blockers: Control systemic hypertension and provide renoprotection, particularly in the presence of diabetes mellitus Dialysis Renal transplantation

Question 515

2 main classes of diuretics used in the management of chronic HTN

Answer 515

1. thiazides 2. potassium sparing drugs

Question 516

Thiazide diuretics (i,e, hydrochlorothiazide) MOA

Answer 516

-cause inhibition of NaCl transport in the distal convoluted tubule -due to inhibition of Na-Cl transport system increase sodium and chloride excretion -by increasing sodium load in the distal renal tubule, they indirectly increase potassium excretion via the sodium/K exchange mechanism

Question 517

Amiloride and Triamterene

Answer 517

block sodium channels in the luminal membrane in the late distal tubule and collecting duct. Such action inhibits the normal movement of Na+ into the cell. Since K+ secretion in the late distal tubule and collecting duct are driven by the electrochemical gradient generated by Na+ reabsorption, K+ (and H+) transport into the urine is reduced. By reducing the net negative luminal charge, amiloride/triamterene administration help conserve potassium. Therefore, they are called "potassium sparing".

Question 518

Carbonic Anhydrase inhibitors

Answer 518

Not used much now Weak diuresis compared to others. Used more in glaucoma to decrease aqueous humor production. Main agent is Acetazolamide (Diamox) Acts in proximal tubule to decrease the conversion of bicarbonate in the tubular fluid to CO2 + H2O, thus blocking reabsorption of bicarbonate, with the concomitant increase in tubular ion load and water loss.

Question 519

Major side effects of thiazide diuretics

Answer 519

hypokalemia metabolic alkalosis (secondary to hypokalemia) electrolyte imbalances hyperglycemia (due to hypokalemic reduction of insulin secretion) hyperuricemia due to inhibition of uric acid secretion in the proximal tubule, which can lead to attacks of gout.

Question 520

high ceiling diuretics

Answer 520

Useful for both left and right ventricular failure. Care must be exercised to avoid excessive diuresis, dehydration, and electrolyte imbalances. Hypokalemia is especially problematic, since many patients are also taking the digitalis glycosides, and this can lead to an increased risk of digitalis toxicity. Torsemide may cause less potassium loss than other loop diuretics.

Question 521

Angiotensin II receptor blockers

Answer 521

newer class of drugs competitive inhibitors of AT1 receptor effects similar to ACE inhibitors, decreasing AT1-mediated vasoconstriction and fluid retention ACE inhibitors also inhibit some bradykinin metabolism, and this may play a role in SE’s of ACE inhibitors. Also, some angiotensin II produced by non-ACE mechanisms approved for use as antihypertensives, but have been used in CHF

Question 522

adverse effects of loop diuretics

Answer 522

Ototoxicity Furosemide (Lasix) and ethacrynic acid (Edecrin) block renal excretion of uric acid by competition with renal secretory and biliary secretory systems. Therefore these agents can precipitate gout. Potassium depletion.

Question 523

loop diuretics

Answer 523

“High-ceiling" loop diuretics acting primarily at the ascending limb of the loop of Henle. The effectiveness of these agents is related to their site of action because reabsorption of about 30 - 40% of the filtered sodium and chloride load occurs at the ascending loop. Distal sites are not able to compensate completely for this magnitude of reduction of NaCl reabsorption. Loop diuretics increase urinary Ca++ in contrast to the action of thiazides. Loop diuretics also increase renal blood flow by decreasing renal vascular resistance. These drugs are rarely used in the management of hypertension because of their short duration of action and the availability of better drugs

Question 524

Main causes of PUD

Answer 524

-an increase in "attack" factors i.e. in colonization by helobacter pylori or increase acid and pepsin secretions-causing erosion, especially in duodenal ulcer -a decrease in "defense" factors i.e. in resistance to acid- peptic attack

Question 525

Zollinger-Ellison syndrome

Answer 525

-much higher than twice normal twice normal due to increased gastrin release

Question 526

2 basic approaches to PUD therapy

Answer 526

1. to decrease the acidity and/or peptic activity of gastric secretions by: -blocking secretion of acid/or pepsin (Decrease attack strength) -neutralization of HCl or inactivation of pepsin -eradicating H. pylori 2. to enhance the resistance of the mucosa or to protect the base of the ulcer from actions of the acid and pepsin

Question 527

Proton pump inhibitors

Answer 527

Omeprazole (Prilosec, Zegerid [w/ NaHCO3]) – available OTC Lansoprazole (Prevacid) – available OTC Dexlansoprazole (Dexilant) Rabeprazole (Aciphex) Esomeprazole (Nexium) – available OTC, (Nexium I.V.) Pantoprazole (Protonix and Protonix I.V.)

Question 528

H2 antihistamines

Answer 528

Cimetidine (Tagamet) Ranitidine (Zantac) Famotidine (Pepcid) Nizatidine (Axid)

Question 529

Antacids

Answer 529

Mg(OH)2 Al(OH)3 CaCO3 NaHCO3,

Question 530

antimuscarinics to treat stomach acidity

Answer 530

Glycopyrrolate (Robinul) Dicyclomine (Bentyl) Methscopolamine Propantheline Bromide

Question 531

ABX used to treat H. pylori infection

Answer 531

Metronidazole (Flagyl) Tetracycline Clarithromycin (Biaxin) Amoxicillin (Multiple brands and Generic)

Question 532

Antidepressants used to treat stomach acidity

Answer 532

tricyclics

Question 533

Proton pump inhibitors

Answer 533

-proton pump involves an H+/K+ ATPase -energy from the hydrolysis of ATP drives H+ into the parietal cell, from which H+ diffuses into the lumen of the stomach -the ATPase appears to be unique and is not known to be in other cells; this may explain why selective inhibitors of the pump are essentially devoid of pharmacological side-effects -because of the irreversible inhibition of the enzyme, profound inhibition of gastric acid secretion (95-100%) occurs that lasts several days -increased risk of exposure of bacterial cells that get into food stuff

Question 534

Omeprazole

Answer 534

prototype inhibitor is a substituted benzimidazole prodrug that is activated at acid pH to a sulfenamide that binds to and irreversible inhibits the H/K ATPase -it takes approx 5 days to synthesize new enzyme and insert it into the membrane. -concern that such prolonged complete suppression may lead to GI bacterial overgrowth and subsequent colonization of the respiratory tract -also, high prolonged doses of omeprazole have been reported to cause GI tumors in rats

Question 535

What is a reversible inhibitor of the pump and gastric acid suppression is not as prolonged not as big concern of bacterial overgrowth risk?

Answer 535

lansoprazole not good for long term tx of ulcers

Question 536

Which drugs depend on acidic pH for their absorption and may significantly be decreased with PPIs?

Answer 536

Ketoconazole Iron salts Digoxin Ampicillin require low pH to be well absorbed doses should be spaced

Question 537

Side effects of PPIs

Answer 537

-headache -diarrhea -abdominal pain -recent discovery that these agents increase risk of heart attacks and bone fractures

Question 538

PPI may inhibit metabolism of other drugs

Answer 538

-phenytoin warfarin diazepam

Question 539

H2 antihistamines has pronounced effects on both acid and pepsin secretion elicited by:

Answer 539

-histamine -gastrin -caffeine -food -insulin -vagus stimulation thus consistent with major role of histamine in acid secretion

Question 540

Pepsin secretion is ________in proportion to the decrease in volume of acid secreted.

Answer 540

decreased

Question 541

do H2 antihistamines directly effect gastrin secretion?

Answer 541

no

Question 542

do H2 antihistamines have a direct effect on GI motility and lower esophageal sphincter pressure?

Answer 542

no

Question 543

H2 antihistamines are most effective when taken when?

Answer 543

bedtime

Question 544

Which drugs decrease B12 absorption and then slow food absorption because of lack of acid?

Answer 544

H2 antihistamines

Question 545

Basal (fasting) and nocturnal acid secretion are potently inhibited by which drugs

Answer 545

H2 antihistamines

Question 546

When do peak blood levels occur in H2 antihistamines

Answer 546

1-2 hours

Question 547

With H2 antihistamiens, they heal duodenal ulcers usually within ____ weeks, usually somewhat longer for gastric ulcers

Answer 547

4-8

Question 548

A significant fraction of gastrin-induced secretion appears to be resistant to blockade by _________ in some patients.

Answer 548

H2 anithistamines

Question 549

OTC indications for H2 antihistamines

Answer 549

-acid indigestion -sour stomach -heartburn

Question 550

what is the prototype drug for H2 antihistamines

Answer 550

Cimetidine (Tagamet)

Question 551

ulcer coating to increase defense (ulcer coating)

Answer 551

-sucralfate (Carafate) -bismuth compounds (pepto-bismol) -Gaviscon

Question 552

Sucralfate (Carafate) structure

Answer 552

-complex of sulfated sucrose and aluminum hydroxide used in treatment of duodenal ulcers for up to 8 weeks and for maintenance therapy of duodenal ulcers

Question 553

Action of sucralfate

Answer 553

-local effect to selectively bind to free protein in the base of ulcer craters -forms a complex which protects from acid, pepsin and bile salts (acids) -absorbs acid and pepsin -gel strongly adheres to ulcers for 6 hours -may stimulate local production of prostaglandin E -may directly absorb bile salts -poorly absorbed systemically and is activated by acid (do not use within 30 minutes of antacids)

Question 554

SE of sucralfate

Answer 554

-metallic taste -nausea -constipationSuc

Question 555

sucralfate may bind some drugs:

Answer 555

-H2 blocker -fluoroquinolones -phenytoin -quinidine -tetracycline -theophylline -these drugs should be given 2 hours before sucralfate

Question 556

Bismuth compounds

Answer 556

-appear to selectively bind to ulcers providing coating and protectiong from acid and pepsin -other mech include stimulating mucus production or increasing prostaglandin synthesis -contraversial as to whether it has some antimicrobial effects

Question 557

Pepto is commonly used for eradicating H pylori when used in combo with:

Answer 557

tetracycline metronidazole

Question 558

Gaviscon

Answer 558

antacid that contains alginate which foams and floats on surface of gastric contents protects the mucosa and impairs gastric reflux so is more useful in treating GERD

Question 559

Misoprostol (cytotec)

Answer 559

-prostaglandin E1 analog that binds to EP receptors resulting in increased mucus and bicarb production and decreased acid production -approved only for ulcer patient who cannot discontinue NSAID use

Question 560

Antacids

Answer 560

-substances that neutralize Hydrogen ion -some may provide mucosal protection and may possibly bind injurious substances -weak bases that react with acid to form salt and water thus neutralizing acid -action is to increase pH of gastric content to 3.5-4.5 which pepsin activity is diminished, -these agents consist of metal salts such as aluminum hydroxide, magnesium hydroxide or trisilicate, calcium carbonate, sodium bicarbonate -number of mEq of HcL that can be brought to pH 3.5 in 15 min is the acid neutralizing capacity

Question 561

Antacid use

Answer 561

commonly used for dyspepsia and are used as adjuncts to other treatment for PUD -do not provide good control of nocturnal secretion -not used extensively for PUD due to high frequency dosing required

Question 562

Magnesium hydroxide

Answer 562

high neutralizing capacity but can cause diarrhea and hypermagnesemia (in patient with renal insufficiency) -forms insolbule salts that act as cathartics and attract fluid into GIT

Question 563

Aluminum hydroxide

Answer 563

high neutralizing capacity but can cause constipation and absorb some drugs and decrease bioavailablilty -can also cause hypophosphatemia

Question 564

calcium carbonate

Answer 564

moderate neutralizing capacity but if taken in large amounts can cause transient hypercalcemia and rebound acid secretion -liberation of CO2 can lead to abdominal distension, nausea, flatulence and belching with acid reflux -large doses can cause milk-alkali syndrome and nephrolithiasis

Question 565

sodium bicarbonate

Answer 565

high neutralizing capacity but should not be used chronically in ulcer patients because of systemic effects-systemic alkalosis, fluid retention etc -also liberates CO@ -acid rebound is high despite good neutralizing capacity

Question 566

Triple therapy for the eradication of H. pylori

Answer 566

(LAC) Lansoprazole, Amoxicillin and clarithromycin for 10-14 days (BMT) bismuth subsalicyclate, metronidazole, and tetracycline for 14 days (OAC) Omeprazole, amoxicillin and clarithromycin for 10 days

Question 567

LES tone can be decreased by:

Answer 567

-smoking -alcohol -caffiene -mint -chocolate

Question 568

_________ decrease LES tone and should never be used for reflux esophagitis.

Answer 568

anticholinergics

Question 569

Which drugs also decrease LES tone:

Answer 569

-theophylline -progesterone -nitrates -CCB

Question 570

Motilin receptors

Answer 570

-stimulate GI peristalsis and pepsin secretion -erythromycin stimulates motilin receptors and may in part explain the diarrhea commonly seen with erythromycin and its analogs

Question 571

Metoclopramide (reglan)

Answer 571

-thought to be 5Ht3 antagonist and has potent antiemetic effect -may also act as Dopamine (D2) antagonist -may also have cholinomimetic effect-it sensitizes intestinal smooth muscle to ach and increases LES tone. These effects result in increased gastric emptying and so can control diabetic -crosses BBB and can cause significant extrapyramidal symptoms

Question 572

SE of metoclopramide

Answer 572

-extrapyramidal symptoms and depression -hyperprolactinemia -nervousness -dystonia -abd cramping -anticholinergic SE

Question 573

Domperidone (Motilium) (non-us)

Answer 573

-D2 antagonist used to treat gastric hypomotility in diabetics -actions similar to those of reglan but does not cross BBB so no anticholinergic effects and better tolerated -both prokinetic and antiemetic properties -used to stimulate lactation

Question 574

N/V believes to be triggered by what

Answer 574

release of serotonin from enterochromaffin cells of SI which then activates 5HT3 receptors on vagal afferents, triggering the vomiting reflex

Question 575

Ondansetron (Zofran)

Answer 575

-can be administered orally or IV and can prevent emesis due to cisplatin or radiation -oral bioavailability of 60% with effective blood levels appearing 30-60 min after administration -metabolized by liver with plasma half =life of 3-- 4 hours -total daily dose of 32 mg -mild SE: headache, constipation, dizziness

Question 576

Which 5HT3 antagonist is only approved for last chance in women with irritable bowel with severe potential gI SE

Answer 576

alosetron (Lotronex)

Question 577

Herbal Antiemetics

Answer 577

-ginger -peppermint -Ajwain (spice in india)

Question 578

Arepitant (Emend)

Answer 578

NK-1 receptor antagonist -effective against chemotherapeutic induced N/V

Question 579

Fosaprepitant

Answer 579

-IV ester form for NK-1 antagonist that is converted to active form in plasma

Question 580

Rolapitant (Varubi)

Answer 580

NK-1 receptor antagonist -good for delayed N/V (2-5 days) after chemotherapy dose -avoid with Thioridizine (potent antimuscarinic) irregular heartbeat risk

Question 581

substance P

Answer 581

-undecapeptide is one of several compounds classified as tachykinins which are agonists at NK1 receptors

Question 582

NK-1 Receptor

Answer 582

-one of several tachykinin receptors in body -G-protein coupled receptor complexes

Question 583

Antiemetic effects of Benzodiazepines

Answer 583

-efficancy derives from sedative, anxiolytic and amnesic properties especially lorazepam and alprazolam can enhance effectiveness of antiemetic regimens

Question 584

lower GI beeding

Answer 584

Below the ligament of Treitz, or bleeding from the jejunum, ileum, colon, or rectum

Question 585

Achalasia

Answer 585

Denervation of smooth muscle in the esophageal sphincter and lower esophageal leading to decreased muscle wall and sphincter relaxation

Question 586

manifestations of GERD

Answer 586

Heartburn, regurgitation of chyme, and upper abdominal pain within 1 hour of eating

Question 586

upper GI bleed

Answer 586

stomach, esophagus, duodenum

Question 587

hiatal hernia

Answer 587

Sliding hiatal hernia – stomach usually only protrudes into chest cavity on swallowing Paraesophageal hiatal hernia – stomach bulge protrudes into chest cavity beside esophagus

Question 588

pyloric obstruction

Answer 588

The blocking or narrowing of the opening between the stomach and the duodenum Can be acquired or congenital

Question 589

S/s of pyloric obstruction

Answer 589

Epigastric pain and fullness nausea succussion splash (sloshing sound in abdomen after expected emptying) vomiting, and with a prolonged obstruction, malnutrition, dehydration, and extreme debilitation

Question 590

intestinal obstruction vs. ileus

Answer 590

An intestinal obstruction is any condition that prevents the flow of chyme through the intestinal lumen or failure of normal intestinal motility in the absence of an obstructing lesion An ileus is an obstruction of the intestines

Question 591

s/s of intestinal obstruction/ileus

Answer 591

Colicky pain, vomiting, distention, hypovolemia, metabolic acidosis

Question 592

simple obstruction

Answer 592

lesion or minor blockadge

Question 593

functional obstruction

Answer 593

loss of function or paralysis commonly seen after surgery, opioids

Question 594

small intestinal obstruction

Answer 594

pain in cramps and spasms with short (minutes) duration

Question 595

large intestinal obstruction

Answer 595

widespread lower abdominal pain, spasms last longer

Question 596

gastritis

Answer 596

inflammatory disorder of gastric mucosa

Question 597

Acute Gastritis

Answer 597

H.Pylori, NSAIDS

Question 598

chronic gastritis

Answer 598

Chronic fundal (fundus-upper region)gastritis Less common but more severe, gastric mucosa degenerates from body to fundus Decreases HCl and intrinsic factor leading to pernicious anemia May be autoimmune, also seen in other autoimmune disorders such as diabetes and Addison’s disease Chronic antral gastritis Much less severe and can be caused by alcohol, NSAIDS, H. pylori, less severe in antrum baecause of heavier protection in antrum Signs and symptoms of chronic gastritis often do not correlate with the severity of the disease

Question 599

curling's ulcers

Answer 599

Ulcers that develop as a result of a burn injury

Question 600

cushing's ulcers

Answer 600

Ulcers that develop due to increased intracranial pressure which stimulates vagal nerve and triggers increased gastric acid secretion

Question 601

Dumping syndrome

Answer 601

Rapid emptying of chyme from surgically created residual stomach into small intestine A clinical complication of partial gastrectomy or pyloroplasty surgery

Question 602

Developmental factors of dumping syndrome

Answer 602

Loss of gastric capacity, loss of emptying control, and loss of feedback control by the duodenum when it is removed

Question 603

late dumping syndrome

Answer 603

Less common, occurs 1-3 hours after eating Due to hypoglycemia secondary to high-carb meal and large insulin secretion Symptoms include weakness, confusion, sweating

Question 604

Marasmus

Answer 604

Protein energy malnutrition seen in absolute food deprivation Results in dry skin, elimination of fat deposits, irritable behavior