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patho final Flashcards

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1
Q

MCV normal finding

A

80-95 - mean corpuscular volume

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2
Q

MCH normal finding

A

27-31 - mean corpuscular hemoglobin

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3
Q

MCHC normal finding

A

32-36 - mean corpuscular hemoglobin concentration

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4
Q

RDW normal finding

A

11-14.5% - red blood cell distribution width

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5
Q

MCV

A

average size of single RBC

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6
Q

MCH

A

average weight of hemoglobin

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7
Q

MCHC

A

average % of hgb within a RBC - can be hypochromic or normochromic

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8
Q

RDW

A

variation of size among RBC

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9
Q

microcytic normochromic anemia is also called

A

megaloblastic

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10
Q

microcytic normochromic anemia labs

A

increased MCV and MCH, normal MCHC, and increased RDW

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11
Q

how do you get microcytic normochromic anemia

A

B12 or folate deficiency

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12
Q

eryptosis

A

premature death of RBC seen in microcytic normochromic anemia

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13
Q

pernicious anemia due to

A

B12 deficiency

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14
Q

pernicious anemia labs

A

increased MCV, increased MCH, and increased RDW

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15
Q

decreased RBC =

A

decreased blood volume (increased plasma volume)

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16
Q

decrease in RBC causes fluid to shift from

A

interstitial space to vascular space because of increased capillary oncotic pressure. this causes the blood to have a decreased viscosity

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17
Q

SV and HR with decreased RBC

A

increased SV and HR

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18
Q

end product of anemia

A

hypoxemia

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19
Q

overall anemia is caused by

A

altered production, blood loss, and increased destruction

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20
Q

cytic refers to

A

size

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21
Q

chromic refers to

A

HGB

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22
Q

absence of intrinsic factor causes

A

B12 deficiency - need intrinsic factor to absorb B12

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23
Q

absence of intrinsic factor can be from

A

congenital, chronic gastritis, or gastric bypass

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24
Q

B12 deficiency anemia involves and destroys the

A

nervous system through myelin degeneration, paresthesias, gait disturbances, spasticity

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25
Q

treatment for pernicious anemia

A

replace b12

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26
Q

b12 can be administered through and will start to work in

A

subcut injections and needs to be continued throughout life. will correct deficiency in 5-6 weeks

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27
Q

if pernicious anemia is not treated

A

will cause death by HF

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28
Q

where is folic acid absorbed from

A

small intestine and stored in the liver

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29
Q

how much folic acid do you need per day

A

200 mg/day

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30
Q

who usually has folic acid deficiency

A

alcoholics or people with crohn’s

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31
Q

manifestations of folic acid anemia

A

cheilosis stomatitis and diarrhea with malabsorption

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32
Q

cheilosis stomatitis

A

inflammation of mouth and lips with crusty bits in corner of mouth

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33
Q

folic acid administration can correct deficiency within

A

1-2 weeks

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34
Q

Iron supplement can correct deficiency within

A

1-2 weeks

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35
Q

iron deficiency anemia caused by

A

chronic blood loss because body isn’t able to recycle lost iron

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36
Q

what type of pts can have chronic blood loss

A

pt with ulcers, Ulcerative colitis, cirrhosis, hemorrhoids, esophageal varies

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37
Q

iron deficiency anemia s/s

A

activity intolerance, difficulty swallowing, geriatric confusion/memory loss

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38
Q

why do iron deficiency anemia pts have a hard time swallowing

A

inflamed cells over esophagus which can lead to cancer of the esophagus

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39
Q

normocytic-normochromic anemias

A

normal size and normal hgb but deficient in number - can be aplastic and hemolytic

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40
Q

things that cause aplastic anemia

A

stem cell deficiency, drug reaction, autoimmune, chronic kidney disease

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41
Q

what can aplastic cause

A

SOB and tachycardia and is associated with thrombocytopenia

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42
Q

hemolytic anemia

A

premature destruction of RBC and is hereditary or acquired

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43
Q

things that cause hemolytic anemia

A

G6PD deficiency, sickle cell, blood transfusion reaction, infection, DIC, prosthetic cardiac valves

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44
Q

administering blood products helps to

A

improve tissue oxygenation, increase oncotic pressure, and act as a plasma expander

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45
Q

assess before blood product admin

A

2 RN check, check history of blood products, volume status, and consent

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46
Q

what to watch for when administering blood products

A

immune response and fluid volume overload

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47
Q

administer blood product with _________ only

A

NS

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48
Q

PRBCs

A

packed red blood cells given if hemoglobin less than 7

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49
Q

leukocytosis

A

too many white blood cells - have a physiologic stressor

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50
Q

leukopenia

A

not enough white blood cells because of radiation, autoimmune, or bone marrow depression

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51
Q

leukopenia puts you at risk for

A

infection

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52
Q

neutropenia defined as

A

less than 1000 and becomes life threatening below 500

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53
Q

too many eosinophils

A

allergen

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54
Q

too many basophils

A

inflammation

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55
Q

lactic acid occurs during

A

inflammation - anerobic metabolism byproduct

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56
Q

procalcitonin shows for

A

bacterial infection

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57
Q

thrombocytopenia defined as

A

platelet count below 150,000

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58
Q

bleeding with minor trauma platelet count

A

50,000

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59
Q

spontaneous bleeding platelet count

A

20,000-15,000

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60
Q

severe bleeding platelet count

A

less than 10,000

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61
Q

thrombocytopenia can occur from

A

rare congenital disorders that cause decreased production, nutritional deficiencies, HIV, cancer, drugs, or increased platelet consumption

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62
Q

heparin induced thrombocytopenia

A

immune mediated heparin reaction - IgG antibodies activate thrombin/platelets and put bodying prothrombin state in which platelets group together

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63
Q

first indicator of heparin induced thrombocytopenia

A

50% reduction of platelet count

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64
Q

things that can happen during heparin induced thrombocytopenia

A

DVT, PE, STEMI, ischemia from clots

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65
Q

treatment of heparin induced thrombocytopenia

A

stop all heparin products and start a alternative anticoagulants. test for anti-hep antibody

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66
Q

disseminated intravascular coagulation

A

widespread activation of coagulation - consumption of platelets, clots black vessels and cut off blood flow to organs, and bleeding occurs because clotting factors are all in the clots

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67
Q

severity of disseminated intravascular coagulation depends on

A

intensity of what is causing it

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68
Q

causes of disseminated intravascular coagulation

A

sepsis, solid tumors, pregnancy complications, hemolytic blood transfusion, trauma

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69
Q

neoplasm

A

tumor can be benign to malignant

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70
Q

carcinoma

A

epithelial (skin,GI)

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71
Q

adenocarcinoma

A

cancer of gland or duct

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72
Q

sarcoma

A

cancer of connective, muscle, bone

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73
Q

lymphoma

A

solid tumor on lymphatic tissue

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74
Q

leukemia

A

hematologic (circulating) not a tumor

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75
Q

BRCA gene

A

breast cancer risk

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76
Q

PSA gene

A

prostate cancer risk

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77
Q

anaplasia

A

loss of cellular differentiation

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78
Q

pleomorphic

A

variability of size and shape

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79
Q

benign cells are

A

same size and shape

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80
Q

benign tumors

A

well defined capsule, not invasive, slow growth, low mitotic index

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81
Q

malignant tumor

A

rapid growth, high mitotic index, not encapsulated, invasive

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82
Q

paraneoplastic syndrome

A

cluster of symptoms triggered by a tumor and is usually the first sign of malignancy

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83
Q

s/s of paraneoplastic syndrome

A

anorexia, weight loss, fatigue, fever, cachexia

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84
Q

cachexia

A

weakness and wasting of the body due to severe chronic illness

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85
Q

pheochromocytomas

A

tumor inside the medulla of adrenal gland that secretes sympathetic hormones

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86
Q

what other syndromes can be seen with paraneoplastic syndrome

A

bushings syndrome, pheochromocytomas, DIC, syndrome of inappropriate antidiuretic hormone secretion (SIADH), hypoglycemia

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87
Q

chemo is more effective on

A

rapidly growing cancer cells

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88
Q

chemo can cause what dose limiting effects

A

organ function decline, extravasation, N/V/D (dependent on severity), myelosuppression (dependent on severity)

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89
Q

myelosuppression

A

bone marrow suppression which causes anemia, thrombocytopenia, and leukopenia

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90
Q

nadir

A

10-28 days after chemo WBC will reach a low and put pt at risk for infection

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91
Q

normal neutrophil count

A

55-70%

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92
Q

critical WBC count

A

2.5 or under

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93
Q

considerations for pt with low immune system

A

reverse isolation, limit visitation, hand washing, oral care, food contamination

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94
Q

what cause shock

A

not enough O2 and glucose, impaired cellular metabolism, and inadequate perfusion

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95
Q

shock responses

A

inflammatory and stress response

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96
Q

progression of shock causes

A

multiple organ dysfunction syndrome (MODS) and

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97
Q

without treatment shock causes

A

overwhelms the bodys compensatory mechanisms through positive feedback loops and causes a downward spiral

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98
Q

describe what impaired oxygen delivery causes during shock

A

without O2 the cell shifts to anaerobic metabolism which causes a depletion of ATP and a dysfunction of Na/K pump. Na/K pump dysfunction causes increased intracellular Na/H2O which causes cellular edema and disruption of cell membrane, which causes the release of destructive lysosomes. lysosomes leak into tissues and cause breakdown, inflammation, and activation of clotting cascade which further impairs O2 use and causes a continuous positive feedback loop

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99
Q

increased lactic acid levels in shock causes

A

decrease in PH (an acidic environment) which causes decreased cell function, repair, and division

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100
Q

complications of shock

A

clotting cascade and inflammation - vasodilation, increased vascular permeability, and infiltration of leukocytes. both these further impair O2 use

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101
Q

complications of inflammatory response during shock

A

DIC, ARDS, and acute tubular necrosis

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102
Q

shock initially is a ____renal problem but as if progresses

A

shock initially is a prerenal problem but as if progresses causes tubules to become necrotic and turns into an intrarenal problem

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103
Q

describe what impaired glucose delivery causes during shock and why it happens

A

compensatory mechanisms during shock cause impaired glucose uptake, and because the body is under stress it has high cortisol, T3, T4, and catecholamines which cause insulin resistance (high glucose levels), increased SVR and HR. cells then shift to gluconeogenesis to generate fuel for the high metabolic state. because proteins are being used in gluconeogenesis they are no longer available to maintain cellular structure, function or repair. As these proteins are being broken down the byproduct is ammonia and urea and with less serum protein there is a shift of fluid which causes decreased osmotic pressure and edema. The end product is a buildup of toxins (metabolic waste products) which further decrease cell function, disrupt the membrane and allow lysosomes to be released. shock then becomes irreversible

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104
Q

treatment for nonspecific shock

A

discover and correct cause, expand intravascular volume, counteract vasodilation, supplemental O2, glucose control

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105
Q

if there is inadequate volume during shock what med will not work

A

vasopressors

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106
Q

MAP equation

A

(2 x diastolic + systolic) / 3

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107
Q

MAP should be

A

60 or 65 for adequate tissue perfusion

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108
Q

causes of hypovolemic shock

A

loss of whole blood, loss of plasma through burns or 3rd spacing, or loss of volume through diaphoresis, diuresis, diarrhea, or emesis

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109
Q

hypovolemic shock begins to develop when intravascular volume has decreased by

A

15%

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110
Q

initially hypovolemic shock is compensated by

A

increased HR and SVR

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111
Q

s/sx of hypovolemic shock

A

thready pulse, poor skin turgor, and oliguria

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112
Q

treatment for hypovolemic shock

A

administer fluid (fill up the tank first)

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113
Q

treatment for hypovolemic shock

A

administer fluid (fill up the tank first)

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114
Q

alpha 1 receptor

A

sympathetic response - vasoconstriction, decreased gastric motility, glycogenolysis (increased glucose)

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115
Q

alpha 2 receptor

A

blocks sympathetic activity

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116
Q

beta 1 receptor

A

positive inotropic, chronotropic, and dromotropic forces and renin

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117
Q

beta 2 receptor

A

dilation of bronchioles and glycogenolysis (increasing glucose)

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118
Q

inotropic

A

force

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119
Q

chronotropic

A

HR

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120
Q

dromotropic

A

electrical

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121
Q

cardiogenic shock causes

A

left CHF, MI, dysrhythmias, pericarditis, PE, tamponade, and drugs

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122
Q

s/sx of cardiogenic shock

A

dyspnea, ALOC, dusky skin, hypotension, oliguria, low motility of GI

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123
Q

cardiogenic shock definition

A

decreased cardiac output and tissue hypoxia in the presence of adequate intravascular volume

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124
Q

decreased CO causes

A

activation of RAAS and ADH to increased blood volume
catecholamine release to increase SVR
increased SV, preload and after load, and HR

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125
Q

increased SV, preload and after load, and HR causes

A

systemic and pulmonary edema, increased myocardial oxygen demand, decreased ejection fraction and BP, decreased tissue perfusion, impaired cell metabolism, and myocardial dysfunction

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126
Q

anaphylactic shock

A

IgE antibody causes degranulation of mast cells (histamine release). This provokes an extensive immune and inflammatory response, including vasodilation (decreased SVR), increased vascular permeability (causes hypovolemia and oliguria), and constriction of extravascular smooth muscle. This causes bronchoconstriction and GI cramps which can cause diarrhea

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127
Q

CO during anaphylactic shock

A

normal to high

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128
Q

treatment of anaphylactic shock

A

histamine blockers, steroids, epi, inhaled beta 2 agonist

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129
Q

septic shock

A

bacteria enters into the bloodstream and release toxins which causes an immune response. macrophages come in to fight and TNF and nitric oxide are released. This cause extreme vasodilation, hypo perfusion, and tachycardia. when body becomes overwhelmed systemic inflammatory response syndrome (SIRS) occurs and leads to wide spread tissue hypoxia and necrosis which leads to shock and MODS

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130
Q

septic shock treatment

A

30 mL/kg crystalloids

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131
Q

neurogenic shock caused by

A

parasympathetic overstimulation and sympathetic under stimulation which can occur from spinal cord injury

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132
Q

what happens during neurogenic shock

A

massive vasodilation, decreased vascular tone, decreased SVR, Bradycardia which causes inadequate cardiac output.

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133
Q

neurogenic shock treatment

A

vasopressors

134
Q

rescue drug for methotrexate

A

leucovorin

135
Q

luecovorin does what

A

converts to active B9 and preserves normal cells but still allows cancer cells to be killed

136
Q

methotrexate can be administered through

A

intrathecal admin - administration for drugs via an injection into the spinal canal

137
Q

acute pain is a response from

A

the sympathetic nervous system

138
Q

chronic pain

A

pain without a sympathetic response

139
Q

endocannabinoids

A

phospholipids - modulate pain, sleep, immune function, appetite, and stress response

140
Q

somatic pain

A

msk pain give NSAIDs

141
Q

visceral

A

organ pain give opioids

142
Q

number one cause of acute kidney injury

A

sepsis because of decrease percussion to the kidney

143
Q

kidney labs during acute kidney injury

A

increased creatinine, increased BUN, decrease GFR

144
Q

signs of acute kidney injury

A

hyperkalemia, hypermagnesemia, hyperphosphatemia, metabolic acidosis

145
Q

normal BUN level

A

8-20

146
Q

normal creatinine

A

0.7-1.4

147
Q

how do you treat prerenal acute renal injury

A

identify cause and treat the cause and increase BP

148
Q

what happens to GFR, renin, ADH, and NA/h2o during prerenal acute renal injury

A

decrease GFR and increased renin and ADH. Na and H2O retention

149
Q

harmful AE from morphine

A

hypotension

150
Q

what electrolyte can cause cardiac arrest if you give it too fast

A

potassium

151
Q

wrong concentration of what electrolyte can put pt into acute exacerbation of heart failure

A

sodium

152
Q

DIC

A

disseminated intravascular coagulation - is a condition in which blood clots form throughout the body, blocking small blood vessels

153
Q

intrarenal acute kidney injury treatment

A

antibiotic to get rid of infection

154
Q

1 body system effected by altered sodium level

A

brain

155
Q

hypokalemia symptoms

A

irregular pulse and dysrythmias with flattened t and u waves, GI upset, and myalgias to paralysis with respiratory failure

156
Q

hyperkalemia

A

peaked Ts with widening QRS, myalgias, paralysis, GI upset

157
Q

hyperkalemia treatment

A

sodium polystyrene sulfonate, calcium gluconate, IV insulin/dextrose, hemodialysis

158
Q

blood in urine =

A

renal stones

159
Q

top causes of chronic kidney disease

A

DM- uncontrolled hyperglycemia - causes glucose to stick to artery wall which cause damage to artery supplying blood to kidney
HTN (systemic), glomerulonephritis, lupus, chronic UTI

160
Q

treatment of chronic kidney disease

A

identification, protection of remaining glomerular function, correct F&E imbalance supplementation, protein restriction, dialysis, and possible renal transplant

161
Q

what medications would you give to chronic kidney disease pt

A

Ace inhibitors/ARBs, glycemic control, antilipemics, make if patient is on nephrotoxic drugs that the benefit of giving the drug outweighs the risk, and supplementation with Ca, vitamin D, and iron

162
Q

osteoarthritis

A

degenerative, low grade inflammatory joint disease

163
Q

what happens to joints during osteoarthritis

A

erosion of cartilage, thickening and inflammation of synovial capsule, osteophytosis, and pain with limited range of motion

164
Q

when cartilage gets broken up the fragments are taken up by the cartilage cells and digested by

A

the cell’s own lysosomal enzymes

165
Q

what 2 things are thought to play a major role in cartilage degradation in osteoarthritis pt

A

proinflammatory cytokines - interleukin 1 and tumor necrosis factor

166
Q

gout

A

syndrome caused by either overproduction or under-excretion of uric acid and is characterized by inflammation and pain in the joints

167
Q

osteoporosis

A

silent progressive bone loss in which pt has more bone resorption and new bone formation

168
Q

postmenopausal induced osteoporosis

A

from estrogen deficiency which causes and abundance of RANKL and decrease influence of OPG, and more bone destroyers than bone formers

169
Q

what does OPG do

A

stops bone resorption

170
Q

where exactly in the kidney does blood filtration take place

A

at the glomerulus

171
Q

what do juxtaglomerular cells do

A

they regulate renal blood flow and systemic blood pressure by secreting renin

172
Q

2 natural (hormonal) antagonists to the RAA system

A

urodilatin and BNP

173
Q

RANKL

A

The interaction of RANK with its ligand (RANKL) has been identified as the final common pathway through which bone resorption is regulated

174
Q

lactic acid is used as a marker for the

A

severity of sepsis

175
Q

GFR of kidney failure

A

below 15

176
Q

GFR of kidney disease

A

15-60

177
Q

what is urea

A

waste product produced from liver breaking down protein

178
Q

How can myoglobin cause infrarenal injury?

A

excess myoglobin may thus cause renal tubular obstruction, direct nephrotoxicity (ischemia and tubular injury), intrarenal vasoconstriction

179
Q

why does chronic kidney disease cause bone pain

A
  • Kidneys activate vitamin D – helps absorb Ca in CKD kidney not activating vitamin D so low calcium and High phosphate levels cause even lower calcium levels because calcium binds to phosphate
  • Hyperparathyroidism
  • Parathyroid gland secrete parathyroid hormone when calcium levels are low
  • Parathyroid hormone indirectly influences osteoclast by stimulating the bones to release calcium into the blood = decreased bone health and possible bone pain
180
Q

what does chronic kidney disease do to CV and pulmonary system

A

causes pulmonary edema, HTN, HF, edema

181
Q

why does chronic kidney disease cause Anemia, epistaxis (nose bleed), bruising

A

because of the reduced erythropoietin secretion and toxins alter platelet function. patient can look pale

182
Q

why does chronic kidney disease cause N/V and anorexia

A

retention of metabolic acids and waste products

183
Q

what type of skin problems can you see on a CKD patient

A

pruritic excoriations, frost, sallow pigmentation, discolored nails

184
Q

CKD and muscles

A

myopathy (muscle weakness) – due to decrease amount of protein

185
Q

why can CKD pt have hypothyroidism

A

Uremia delays the response of thyroid stimulating hormone receptors and Ts levels are often low

186
Q

insulin resistance in chronic kidney pt

A

Related to proinflammatory cytokines and alterations in adipokines (causes high leptin and low adiponectin)

187
Q

what happens to your immune system with CKD

A

Immune system is suppressed due to uremia (high level of urea in blood)

188
Q

what structure actually produces the urine

A

nephrons

189
Q

what shows up in urine during CKD

A

protein and blood

190
Q

why do CKD pt get metabolic acidosis

A

because there is a diminished ability to excrete H+ and generate bicarb which leads to acidosis

191
Q

EKG during hypokalemia

A

long QU interval and prominent U waves

192
Q

EKG during hyperkalemia

A

peaked T waves

193
Q

EKG during hypocalcemia

A

QT prolongation

194
Q

EKG during hypercalcemia

A

shortening of the ST segment

195
Q

steps to late stage of CKD

A
  1. HTN in arteries going to the kidney which causes release of renin which causes more HTN and over time will cause vessel thickening and narrowing which will lead to glomerulosclerosis.
  2. sclerosis causes ischemic injury and nephron loss
  3. nephrons are compensating for other lost nephrons so there is glomerular hyperfiltration that is tolerated during early stages, but not in late
  4. hyperfiltration causes more sclerosis from the pressure
  5. more loss if nephrons
  6. nephrons can not compensate any more and you have a decrease in GFR
196
Q

what does gastrin do?

A

stimulates gastric glands to secrete HCl, pepsinogen, and histamine

197
Q

what does acetylcholine do to the stomach

A

stimulates the release of pepsinogen and acid secretion

198
Q

what do prostaglandins do

A

regulate perfusion to stomach, regulates mucus to release bicarb, and controls acid amount secreted by parietal cells

199
Q

what do the parietal cells do

A

secrete HCl and intrinsic factor

200
Q

what happens if your stomach is empty but your stressed so your stomach is still secreting gastrin and histamine

A

gastrin stimulates stomach to release pepsinogen which is turned into pepsin and can cause ulcers

201
Q

what is intrinsic factor needed for

A

absorption of B12

202
Q

what happens in your stomach when you eat food

A

Food stimulates gastrin
Gastrin stimulates parietal cells to release HCl, intrinsic factor, histamine, and stimulates chief cells to release pepsinogen
Histamine stimulates more acid secretion
Pepsinogen - breakdown protein and turn into pepsin
Intrinsic factor needed for B12 absorption

203
Q

hematochezia vs melena

A

both are a type of GI bleed. hematochezia is bright red filled with blood clots, not digested blood- shows problem in lower GI. Melena is coffee ground - dark, digested blood from upper GI

204
Q

what meds can people take for gastritis

A

PPIs or H2 blockers

205
Q

how duodenal ulcers form

A

usually from H. Pylori which activates T and B lymphocytes and neutrophil infiltration and release of inflammatory cytokines which damage the gastric epithelium. they can also occur form acid and pepsin not deactivating when entering the duodenum

206
Q

gastric ulcer caused by

A

a break in the mucosa that allow hydrogen ions to diffuse through the mucosa which causes damage and release of histamine

207
Q

the release of histamine during gastric ulcers cause

A

increase blood flow from vasodilation and increased permeability. this all causes loss of plasma proteins and damaged vessels which causes bleeding

208
Q

H2 receptor antagonist do what

A

decrease acetylcholine and gastrin. increases the ph and reduces the H+ secretion from the parietal cells

209
Q

nursing consideration for Pepcid

A

H2 receptor antagonist - dilute with 5-10 ml of NS and push over 2 minutes or can cause hypotension

210
Q

liver metabolizes

A

glucose and stores it as glycogen and converts glycogen to glucose

211
Q

what happens with glucose in liver disease patients

A

they can get hepatic diabetes from chronic high blood glucose levels

212
Q

what is the byproduct of protein metabolism

A

ammonia

213
Q

what does the liver do with ammonia

A

converts it to urea so if the liver is not functioning properly a build up of ammonia can occur

214
Q

liver stores

A

vitamins B12, A, C, E, D, and K

215
Q

vitamin D does what

A

helps absorb calcium

216
Q

vitamin K does what

A

helps the clotting process

217
Q

liver helps with the production of

A

blood plasma proteins

218
Q

portal hypertension

A

abnormally high blood pressure in the portal venous system caused by resistance to blood flow

219
Q

intrahepatic causes of portal hypertension

A

inflammation, fibrosis, and vascular remodeling that occur from cirrhosis or hepatitis

220
Q

post hepatic causes of portal hypertension

A

impaired pumping of the heart or obstruction from Right HF or thrombus

221
Q

consequences of long term portal hypertension

A

varices, splenomegaly, hepatopulmonary syndrome, portopulmonary hypertension

222
Q

most common symptom of splenomegaly

A

thrombocytopenia (low platelets)

223
Q

hepatopulmonary syndrome

A

shunting occurs because pressure causes new vascular pathway and this new pathway does not pass the alveoli to obtain new oxygen. when the blood that went through the shunt meets up with the oxygenated blood that went through normal pathway the overall blood oxygen level is lower than if there wasnt a shunt. This causes hypoxemia

224
Q

factor that contribute to the development of ascites

A

decreased synthesis of albumin by the liver, portal hypertension, and splanchnic arterial vasodilation

225
Q

what does increased nitric oxide do

A

can decrease effective circulating blood volume which activates RAAS (aldosterone) and antidiuretic hormone, which promotes renal sodium and water retention and overall accelerates portal hypertension and ascites

226
Q

hepatic encephalopathy

A

complex neurologic syndrome where toxins effect neurotransmission because the liver is not able to convert ammonia to urea in its toxic state

227
Q

jaundice results from either

A

obstructive or hemolytic cause

228
Q

extrahepatic causes of jaundice

A

liver still working but bilirubin accumulation because gallstone blockage of bile flow- considered conjugated

229
Q

conjugated

A

hepatocytes functioning so something else is causing the problem

230
Q

unconjugated

A

hepatocytes not functioning so they are the cause of the problem

231
Q

liver labs will be normal in what type of jaundice

A

extrahepatic jaundice

232
Q

fibrosis in the liver of cirrhosis patients is a consequence of

A

infiltration of leukocytes and release of inflammatory mediators

233
Q

ulcerative colitis is mainly in the compared to crohn’s which can be

A

ulcerative colitis is continuous lesions that occur mainly in the large intestine while Crohn’s has skip lesions that can occur anywhere from mouth to anus

234
Q

treatment of ulcerative colitis vs Crohn’s

A

ulcerative colitis is cured with surgery of taking out the entire colon. Crohn’s is not curable and is managed with surgery

235
Q

excessive cortical =

A

Cushing syndrome

236
Q

excessive ACTH

A

Cushing disease

237
Q

what does cortisol do to our bodies

A

increases blood pressure and cardiac output, increases blood levels of amino acids, and decreases luteinizing hormones, estradiol, and testosterone

238
Q

cause of cushing disease

A

caused by a tumor either in pituitary or adrenal

239
Q

cause of Cushing syndrome

A

excessive/long term steroid use or can happen in people with long term high levels of stress

240
Q

stress hormones do what to our BP and glucose

A

they are vasoconstrictors so will increase BP and increase blood glucose levels

241
Q

negative feedback loop for adrenal gland regulation

A

it begins when low circulating corticosteroid hormones are noticed by the hypothalamus or when stress is present. hypothalamus responds by releasing corticotropin releasing hormone which causes anterior pituitary to release adrenocorticotropic hormone (ACTH), this stimulates adrenal cortex to release cortisol. once the threshold of corticosteroids is reached the hypothalamus inhibits the release of corticotropin releasing hormone (CRH).

242
Q

glucocorticoid function

A

carbohydrate metabolism, protein breakdown in the muscle tissue, immune/inflammatory suppression, inhibition of bone formation, nerve function depression, and increase effect of catecholamine response

243
Q

mineralocorticoid function

A

sodium retention, potassium/H+ loss, BP control, increase cardiac contraction, increase systemic vascular resistance, and decrease fibrolysis

244
Q

calcitonin is secreted by the thyroid when

A

circulating calcium levels are too high

245
Q

negative feedback loop of the thyroid gland

A

when circulating thyroid hormones are low the hypothalamus releases thyroid releasing hormone (TRH), this stimulates the anterior pituitary gland to secrete thyroid stimulating hormone (TSH), this stimulates the thyroid to release T3 and T4, T3 and T4 bind to proteins but once the unbound amount of circulating T3 and T4 levels are sufficient the hypothalamus halts the release of thyroid releasing hormone

246
Q

function of T3 and T4

A

regulates protein, fat, and carbohydrate catabolism, metabolic rate, and body heat production. maintains growth hormone secretion, cardiac rate, force, output, secretion of GI tract, and calcium mobilization. affects RR, RBC production, and CNS development

247
Q

what happens with weight during cushing syndrome

A

weight gain with a redistribution of fat

248
Q

what happens with glucose in Cushing syndrome

A

glucose intolerance occurs because of cortisol induces insulin resistance and increased gluconeogenesis

249
Q

what does cushing’s syndrome do to the integumentary system

A

weakens the integumentary system due to loss in collagen which causes the skin to be thin and causes capillaries to become weaker and seen through the skin. this amounts for striae and bruising

250
Q

what does protein wasting cause and what syndrome causes it

A

protein wasting occurs in cushing syndrome from the catabolic effect of cortisol. it causes muscle loss, bone wasting, and is the cause of the weakened integumentary system too

251
Q

bone wasting causes

A

increase fracture risk, increase risk of osteoporosis, hypercalciuria, and risk of stones

252
Q

the elevated levels in cushing syndrome will cause

A

vasoconstriction, HTN, increase risk of infection, mental status change in up to 50% of pt, and mineralocorticoid effects such as water and sodium retention, and increased adrenal androgen

253
Q

treatment for cushing syndrome

A

managing hyperglycemia, HTN, hypokalemia, and metabolic alkalosis. possible stress dosing. radiation, surgery, gradual cessation of steroids, help with the patients with disturbed body image

254
Q

hyposecretion of cortisones and aldosterone

A

Addison disease

255
Q

lab levels during Addisons disease

A

low cortisol, low aldosterone, high ACTH because of the loss in negative feedback. low sodium, low glucose, fluid volume deficit, increased potassium, increased BUN, and high WBC because autoimmune

256
Q

signs and symptoms of Addison disease

A

weight loss, fatigue, N/V/D, skin changes, infection

257
Q

treatment of Addison disease

A

lifetime fludrocortisone and glucocorticoid, a minimum of 3400 mg of sodium per day, and low stress

258
Q

adrenal crisis can be caused by

A

Addison disease or stopping exogenous steroids too fast

259
Q

what occurs during an adrenal crisis

A

hypotension, vascular collapse, hypovolemic shock

260
Q

priority treatment for Adrenal crisis

A

administer cortisol

261
Q

hyperthyroid labs

A

low TSH and high T3 and T4

262
Q

hypothyroid labs

A

high TSH and low T3 and T4

263
Q

thyrotoxic storm labs

A

normal TSH, super high T3 and T4 because brain hasn’t turned TSH off yet - this is an acute problem

264
Q

graves disease

A

primary hyperthyroidism due to autoimmune disease

265
Q

signs of graves disease

A

exophthalmos and pretrial myx-edema

266
Q

hyperthyroidism treatment

A

antithyroid drugs, surgery - removal of the thyroid, radioactive iodine therapy, beta blockers, and symptom relief

267
Q

thyrotoxic crisis treatment

A

anti thyroid drug, beta blockers for control of cardiovascular symptoms, steroids

268
Q

manifestation of hypothyroidism

A

low metabolic rate, cold intolerance, lethargy, bradycardia, goiter

269
Q

secondary hypothyroidism causes

A

traumatic brain injury, Subarachnoid hemorrhage, or pituitary tumors or infarction

270
Q

myxedema coma causes

A

decrease LOC, hypotension, hypoglycemia, hypothermia, hypoventilation which causes hypoxia and can lead to lactic acidosis

271
Q

folliculitis

A

infection of the hair follicle that is caused by bacterial, fungal, and viral infection but S. aureus is the predominant culprit

272
Q

furuncles

A

“boils” - folliculitis that is spread to dermal tissue

273
Q

carbuncle

A

collection of infected hair follicles that extends into the subcutaneous tissue

274
Q

characteristics of carbuncle

A

systemic complications - fever, chills, weakness

abscess may develop

275
Q

Cellulitis

A

infection of the dermis and subcutaneous tissue usually caused by S. aureus

276
Q

what is needed for cellulitis

A

systemic antibiotic

277
Q

treatment for CRE

A

only 2 antibiotics are able to treat it but one of them had a “all-cause mortality” BBW

278
Q

When is a mineralocorticoid released by the adrenal cortex

A

Mineralocorticoid is released by the adrenal cortex in response to angiotensin II, but overall is stimulated by low sodium and water depletion, increased potassium levels, and diminished blood volume.

279
Q

You notice your patient is exhibiting itching, throat swelling and a fast irregular pulse. Which three medications would you anticipate administering swiftly

A

Epinephrine, diphenhydramine, and famotidine

280
Q

Name one response the GI system has to a release of serotonin

A

Serotonin causes vasodilation in the gut.

281
Q

Identify the ABG abnormality associated with vomiting/ diarrhea, respectively.

A

Vomiting is associated with metabolic alkalosis and Diarrhea is associated with metabolic acidosis.

282
Q

List the 7 (yes, 7) main functions of the liver.

A
  1. Formation and secretion of bile
  2. Metabolism of bilirubin
  3. Stores blood, syntheses of clothing factors, and bile production
  4. metabolism of fats and nutrients and releases and absorbs glucose and stores glycogen
  5. metabolic detoxification
  6. storage of vitamins and minerals
  7. synthesis of thrombopoietin
283
Q

how does the stomach lining survive through the acidic environment

A

prostaglandins are simulated to secrete mucus that creates a barrier to protect the stomach

284
Q

neurotransmitter released when food enter into the duodenum

A

serotonin which causes and increase in GI mobility and vasodilation in gut

285
Q

minimum inhibitory concentration

A

lowest amount of antibiotics needed to kill a bacteria includes how long the patient is on and the concentration

286
Q

treatment for inflammatory bowel disease

A

corticosteroids to keep inflammation down now, biologics, immunomodulators- keep inflammation down in future, antibiotics, and treat symptoms -anti-diarrheal and nutritional deficiencies (anemia)

287
Q

bacteriostatic

A

inhibit growth of bacteria

288
Q

general anemia patho

A

decreased RBC which causes fluid to move into vascular space and blood gets thiner which causes blood to move faster and more turbulent through the vessels. This causes tress on the heart and increases stroke volume and heart rate. end result can be high output heart failure. blood will flow to vital organs and there will be a decreased blood flow to the kidney which will cause activation of RAAS and even more fluid build up.

289
Q

general signs of anemia

A

lethargy, pale/jaundice, abd pain/N/V due to decreased blood to GI, SOB, low fever, impaired healing, tachycardia, HF, difficulty walking, paresthesias of hands and feet because of myelin degeneration in B12 deficient anemia

290
Q

iron supplements

A

Ferrous sulfate, iron dextran, and iron sucrose

291
Q

ferrous sulfate

A

oral - no dairy or antacids. OJ increases absorption. sit upright for 30 min

292
Q

Iron dextran

A

IV - need test dose before, watch for anaphylaxis and hypotension

293
Q

iron sucrose

A

IV - don’t need test dose before. watch for hypotension

294
Q

macrocytic normochromic anemias

A

pernicious and folic acid deficient

295
Q

microcytic hypochromic anemia

A

iron deficiency

296
Q

normocytic normochromic anemias

A

aplastic and hemolytic

297
Q

if pt is on furosemide what else should they be on

A

K supplement

298
Q

opioid reversal

A

naloxone

299
Q

MG sulfate

A

IV - can cause tornadoes de pointes (ribbon shape on EKG)

300
Q

MG oxide

A

supplement (oral)

301
Q

MG citrate

A

laxative

302
Q

phenazzopyridine (Pyridium)

A

for pain caused by UTI

303
Q

cyclosporin

A

med given for organ rejection prevention

304
Q

antibiotics given for IBS

A

ciprofloxacin or flagyl

305
Q

pharmacological treatment for IBS

A

corticosteroids, biologics (anti-ca, anti-TNF), immunomodulators, antibiotics, and antidiarrheals

306
Q

antidiarrheals

A

non-opiate: belladonna alkaloid (donnatal elixir)

opiate: lomotil and Imodium

307
Q

psyllium (Metamucil)

A

bulk forming laxative

308
Q

glucocorticoids

A

hydrocortisone, solu-medrol, prednisone, dexamethasone

309
Q

mineralcorticoid

A

fludrocortisone for Addisons disease

310
Q

antithyroid drugs

A

methimazole (tapazole) and PTU

311
Q

epinephrine does what

A

vasoconstrictor and bronchodilator - nonselective adrenergic agonist

312
Q

Bactrim

A

sulfonamide for UTI but has hypoglycemic effect with sulfonylureas, encephalopathy effect with phenytoin, and nephrotoxic with cyclosporin

313
Q

PCN G IM

A

uncomplicated syphilis

314
Q

pipercillin/tazzobactam (Zosyn)

A

beta lactase inhibitor for H-A infection, PNA, or sepsis

315
Q

cefazolin (ancef)

A

1st generation cephalosporin for surgical prophylaxis - has most gram positive coverage

316
Q

cefepime (maxipime)

A

4th generation cephalosporin for complicated UTI, PNA and skin infection

317
Q

ceftaroline (Teflaro)

A

5th generation cephalosporin for MRSA and PNA

318
Q

meropenem (merrem)

A

carbapenem antibiotic - for MRSA PNA sepsis UTI

319
Q

ertapenem (invanz)

A

carbapenem antibiotic - for MRSA PNA sepsis UTI

320
Q

erythromycin

A

macrolide antibiotic - for eye/skin infection, chlamydia, gonorrhea - causes increased GI motility and has more AE than azithromycin

321
Q

tobramycin

A

aminoglycocide antibiotic - for resistant gran negative bacteria but can be oto/nephro/neuro toxic

322
Q

what is different in septic shock metabolism

A

plasma protein breakdown includes the metabolism of immunoglobulins which impairs the immune system function when it is most needed.

323
Q

septic anaerobic metabolism

A

protein metabolism releases alanine which converts into pyretic acid which is sepsis is converted into lactic acid and worsens metabolic acidosis and glucose metabolism

324
Q

Identify 2 key functions of the hematologic system.

A

Hematologic system provides oxygen and nutrients to tissues and help defend against foreign invaders. They also help us repair from traumatic injury.

325
Q

Identify 2 inorganic or organic molecules that albumin can transport.

A

Albumin can transfer drugs and other blood components. These blood components include vitamins, hormones, and lipids.

326
Q

Where are the sites of active red bone marrow? (provide two specific bones)

A

Sites are in flat bones such as the skull and vertebrae.

327
Q

What is the normal hematocrit for both men and women

A

48% of blood volume in men

42% of blood volume in women

328
Q

Why do patients with sickle cell anemia have a difficult time maintaining oxygenation?

A

Patients with sickle cell anemia have a crescent shaped red blood cell. This makes it difficult for the red blood cells to maintain a good flow, which overall decreases the ability to maintain oxygenation. These patients need a steady flow of oxygen.

329
Q

Name three stimuli for accelerated erythropoiesis.

A

Stimuli that accelerate erythropoiesis are decline in arterial oxygen levels and tissue hypoxia, high altitude, anemia, and pulmonary disease.

330
Q

Eosinophils release which 3 enzymes that help control inflammatory processes?

A

Eosinophils release prostaglandins, leukotrienes, and histamine.

331
Q

Lymphocytes are the primary cells in which type of immunity?

A

Lymphocytes are the primary cells in adaptive immunity.

332
Q

Patients are usually asymptomatic until platelet counts drop below _______ and spontaneous bleeding usually does not occur until platelet counts are below ________.

A

Patients are usually asymptomatic until platelet counts drop below 100,000 and spontaneous bleeding usually does not occur until platelet counts are below 20,000.

Nursing school level 2 (15 decks)

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