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Pathophysiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Posterior pituitary secretes these hormones

A

ADH and Oxytocin

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2
Q

Causes of SIADH:

A
  • Ectopic excretion of ADH by tumor cells; also meningitis, brain injury, and stroke (most common)
  • Surgery: following pituitary surgery stored ADH is released in unregulated fashion (5-7 days)
  • After treatment with a variety of drugs (e.g., pulmonary disease, psychiatric disease, etc)
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3
Q

Features of SIADH:

A

water retention and solute loss

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4
Q

Manifestations of SIADH:

A

thirst, dyspnea on exertion, fatigue, dulled consciousness progressing to abdominal cramps, vomiting, confusion and seizures

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5
Q

Diseases of the Posterior Pituitary are:

A

SIADH and Diabetes Insipidus

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6
Q

Diabetes Insipidus is caused by:

A

insufficient activity of ADH, leading to polyuria and polydipsia; two ways to have DI

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7
Q

Two ways to have Diabetes insipidus:

A

1) neurogenic

2) nephrogenic

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8
Q

Neurogenic DI

A

lesion on hypothalamus or posterior pituitary interferes with ADH synthesis, transport or release; problem with the neurons that make/release it

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9
Q

Nephrogenic DI

A

Insensitivity of renal tubule to ADH; usually acquired/congenital; produce enough ADH but tubules aren’t responding to it

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10
Q

Psychogenic DI

A

When a person has an extremely large fluid intake it results in a partial resistance to ADH; more easily reversible than other two forms of DI

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11
Q

Growth hormone and prolactin are regulated by what brain structure?

A

Anterior pituitary

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12
Q

What is acromegaly?

A

results from continuous exposure to high levels of GH; almost always caused by a GH-secreting pituitary adenoma; usually occurs in adults 40-59 years old

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13
Q

Most common cause of acromegaly?

A

GH-secreting pituitary adenoma

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14
Q

Visible physical characteristics of acromegaly

A

soft tissues grow, enlargement of hands and feet, bones of face and skull enlarge, teeth are splayed

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15
Q

Cardiovascular effects of acromegaly

A

enlargement of heart, accelerated atherosclerosis leading to early death, high risk for cardiovascular disease due to high BP

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16
Q

In acromegaly, blood sugars are usually high or low?

A

high, most are diabetic

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17
Q

What is giantism?

A

Excessive skeletal growth due to increase GH secretion in children whose epiphyseal plates have not yet closes

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18
Q

What is a prolactinoma?

A

a pituitary tumor that secretes prolactin; most common hormonally active pituitary tumors leading to prolactinemia

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19
Q

What does prolactin effect in women?

A

breast development and tissues that produce milk; inhibits estrogen

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20
Q

What does prolactinoma cause in women?

A

amenorrhea, glactorrhea, hirsutism, osteopenia

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21
Q

What does prolactinoma cause in men?

A

hypogonadism and erectile dysfunction

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22
Q

Thyroid stimulating hormone (TSH) is secreted by what area of the brain?

A

anterior pituitary

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23
Q

What are the 2 alterations of thyroid function?

A

hyperthyroidism and hypothyroidism

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24
Q

What is hyperthyroidism?

A

When TSH is low, TH is high; metabolism high, high energy, lower weight; thyrotoxicosis-higher levels of TH from any source

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25
Q

What is hypothyroidism?

A

TSH is high; TH is low; low metabolism, fatigue; congenital or acquired

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26
Q

TH inhibits growth because….

A

For GH to be active, TH has to be effective. Without stimulation of GH by TH, the person will stay short in stature.

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27
Q

Graves disease is a form of hyper/hypo-thyroidism?

A

Hyperthyroidism; autoimmune; most common form of hyperthyroidism; IgG binds to where TSH does which produces abnormal stimulation of thyroid gland by IgG antibodies or causes exophthalmos, irritability, weight loss, and fatigue

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28
Q

What is congenital hypothyroidism?

A

Present at birth but appears normal because of maternal TH secretion; most common cause of preventable mental retardation; cretinism

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29
Q

What is cretinism?

A

Lack of TH leading to inefficiency of GH, causing decreased brain development, decreased physical growth, and mental retardation

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30
Q

What is acquired hypothyroidism?

A

slowing down of metabolic processes with age; myxedema; caused by destruction or dysfunction of thyroid gland; secondary cause may be impaired pituitary

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31
Q

myxedema

A

nonpitting mucous edema; hypothyroidism symptom

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32
Q

Hashimoto’s Disease

A

autoimmune; causes destruction of thyroid gland; acquired hypothyroidism

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33
Q

Parathyroid hormone (PTH) stimulates

A

calcium secretion

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34
Q

What is hyperparathyroidism?

A

Make too much PTH, usually due to tumor and increase calcium in the blood

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35
Q

Primary hyperparathyroidism

A

PTH secretion increased; high levels of calcium in blood and urine; fatigue, depression, anorexia

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36
Q

Secondary hyperparathyroidism

A

compensatory response to chronic hypocalcemia due to decreased renal function and lack of Vitamin D production; PTH elevated; calcium levels low or normal

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37
Q

Clinical manifestations of hyperparathyroidism

A
  • hypercalcemia (asymptomatic or bone resorption)
  • hypercalciuria metabolic acidosis, alkaline urine, formation of calcium stones
  • fatigue, depression, anorexia
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38
Q

What is hypoparathyroidism?

A

make too little PTH, most common cause is damage to parathyroid glands during thyroid surgery

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39
Q

Clinical manifestations of hypoparathyroidism:

A

-hypocalcemia (lowered threshold for nerve and muscle excitation)

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40
Q

hypocalcemia can cause:

A

muscle spasm, hyper-reflexia, convulsions, asphyxiation, numbness, dysrhythmias, low BP, dry skin, hair loss, cataracts, cone deformities

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41
Q

What is diabetes mellitus?

A

chronic hyperglycemia along with disturbances of carbohydrate, fat, and protein metabolism; number 5 cause of preventable death

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42
Q

4 factors of diabetes mellitus diagnosis:

A

1) >1 elevated fasting plasma glucose level
2) elevated plasma glucose levels in response to oral glucose tolerance test
3) classic symptoms of polydipsia, polyphagia, and polyuria
4) glycosylated hemoglobin (HgA1c)

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43
Q

What is Type I diabetes mellitus?

A

Insulin-dependent; lack of insulin and relative excess of glucagon; autoimmune; cells attack cells of the pancreas; must have genetic propensity and encounter a trigger; immune system starts seeing beta cells as foreign; sugar lost in urine due to excessive amounts that can’t all be reabsorbed

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44
Q

epidemiology of Type I DM

A

most commonly diagnosed in those younger than 18

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45
Q

etiology of Type I DM

A

beta cells destroyed due to autoantibodies

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46
Q

manifestations of Type I DM

A

polydipsia because of polyuria resuting from osmotic diuresis, weight loss and polyphagia; ketoacidosis due to increased metabolism of fats and proteins (think low-carb diets)

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47
Q

What is Type II Diabetes Mellitus?

A

non-insulin dependent; most prevalent form of DM

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48
Q

Epidemiology of Type II DM

A

Native Americans, Hispanics, and blacks; most over 40 and many are obese

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49
Q

Etiology of Type II DM

A
  • impaired beta cell function; insulin reduction
  • peripheral insulin resistance
  • increased hepatic glucose production
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50
Q

peripheral insulin resistance

A

obesity promotes insulin resistance becasue the cell receptors modify shape with increased/decreased size of cell… weight loss important (T2DM)

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51
Q

increased hepatic glucose production

A

liver releases too much glucose; too much glucagon produced, insulin levels go up (T2DM)

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52
Q

Manifestations of Type II DM

A

nonspecific; pruritis, recurrent infections, visual changes, paresthesias, polyuria, polydipsia

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53
Q

Three ways to manage diabetes mellitus:

A
  • dietary: restrict calories and balance macro’s
  • exercise
  • oral antidiabetic agents: increase peripheral glucose uptake; increase insulin secretion by pancreas; decrease glucose output by the liver
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54
Q

Microcytic

A

small cell

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55
Q

normocytic

A

normal cell

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56
Q

macrocytic

A

large cell

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57
Q

normochromic

A

normal color

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58
Q

hypochromic

A

decreased color (due to decreased hemoglobin in the cell)

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59
Q

mean corpuscular volume (MCV)

A

how big the cell is

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60
Q

mean corpuscular hemoglobin concentration (MCHC)

A

Volume of hemoglobin in a cell. Influences cell color

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61
Q

hemoglobin

A

protein in RBC’s that carries oxygen

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62
Q

Causes of anemia

A

low RBC numbers, low hemoglobin, or both

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63
Q

Manifestations of anemia

A

reduced oxygen carrying capacity of the blood resulting in tissue hypoxia

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64
Q

What is anemia?

A

A condition marked by a deficiency of red blood cells or of hemoglobin in the blood, resulting in pallor and weariness

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65
Q

Mechanism of anemia

A
  1. fluid moves into blood vessels
  2. blood vessels dilate resulting in increased HR
  3. increased respirations
  4. decreased blood flow to kidneys activating renin-angiotensin mechanism
  5. pale skin, mucous membranes, lips, nail beds, and conjunctivae
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66
Q

Macrocytic-Normochromic anemias

A

large, normal color cells; due to ineffective RBC DNA synthesis resulting in cells that die prematurely; number of circulating RBC’s is lower

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67
Q

Types of Macrocytic-Normochromic anemias (x2)

A
  1. Vitamin B12 deficiency anemia

2. folic acid deficiency anemia

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68
Q

Vitamin B12 deficiency anemia (pernicious anemia-PA)

A

Macrocytic-Normochromic anemia; Vitamin B12 is necessary for DNA synthesis; can only get Vit B12 from animal products

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69
Q

Risk factors for vit B12 deficiency anemia

A
  • over 30

- Northern european, black, hispanic

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70
Q

Cause of Vit B12 deficiency anemia

A
  • Deficiency of intrinsic factor (IF), which is required for absorption of vitamin B12
  • may be congenital, due to gastric mucosal atrophy (often the result of an autoimmune disorder resulting in destruction of parietal cells which secrete gastric acid in the stomach)
  • heavy alcohol consumption
  • cigarette smoking
  • hot tea drinking
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71
Q

manifestations of vit B12 deficiency anemia

A
  • weakness
  • fatigue
  • paresthesias of feet and fingers
  • difficulty walking
  • loss of appetite
  • sore tongue that is smooth and beefy red
  • develops slowly over 20-30 years
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72
Q

Vit B12 deficiency anemia can cause this if untreated

A

heart failure

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73
Q

Folic acid deficiency anemia

A

macrocytic-normochromic anemia; Folic acid (folate) is essential for RNA/DNA synthesis in RBC

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74
Q

Folate is absorbed and stored where?

A

Absorbed in small intestine, stored in the liver

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75
Q

manifestations of folic acid deficiency anemia

A
  • weakness
  • fatigue
  • loss of appetite
  • sore tongue that is smooth and beefy red
  • no neurologic symptoms
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76
Q

Common causes of folic acid deficiency anemia

A
  • alcoholism

- malnourishment

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77
Q

Microcytic-hypochromic anemias

A

small, pale cells; contain abnormally reduced amounts of hemoglobin

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78
Q

iron deficiency anemia (IDA)

A

microcytic-hypochromic anemia; lack of color due to lack of iron, which decreases amount of oxygen in cell

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79
Q

types of microcytic-hypochromic anemias (x2)

A

1) iron deficiency anemia (IDA)-most common in the world

2) Sideroblastic anemia

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80
Q

IDA is most commonly found in these people:

A
  • pregnant women
  • adolescents
  • children
  • elderly
  • those with chronic blood loss of as low as 2-4 mL/day
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81
Q

Causes of IDA in men

A

ulcers, Hiatal hernia, espophageal varices, cirrhosis, hemorrhoids, ulcerative colitis, cancer

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82
Q

Causes of IDA in women

A

excessive menstrual bleeding

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83
Q

Causes of IDA in both men and women

A

medications that cause GI bleeding, decreased iron absorption, insufficient intake, pica (eating non-food items)

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84
Q

Early S&S if IDA:

A
  • fatigue
  • weakness
  • SOB
  • pale ear lobes, palms, and conjunctiva
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85
Q

Long-term S&S of IDA:

A
  • Nails: brittle and spoon-shaped (koilonychia)

- tongue papillae atrophy

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86
Q

Sideroblastic anemia

A

microcytic hypochromic anemia; due to inefficient iron uptake, resulting in abnormal hemoglobin synthesis; ringed sideroblasts that contain iron granules that have not been synthesized into hemoglobin; increased tissue levels of iron

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87
Q

acquired Sideroblastic anemia

A

due to drug reaction, alcohol, lead

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88
Q

hereditary Sideroblastic anemia

A

x-linked recessive in males

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89
Q

reversible Sideroblastic anemia

A

associated with alcoholism and results from deficiencies of folate

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90
Q

manifestations of Sideroblastic anemia

A
  • hepatomegaly
  • splenomegaly
  • bronze-tinted skin
  • cardiac arrhythmias
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91
Q

normocytic-normochromic anemias

A

normal size and color; less common; not enough RBC’s but enough Hemoglobin; pancytopenia

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92
Q

pancytopenia

A

decrease in all number and types of cells

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93
Q

aplastic anemia

A

normocytic-normochromic anemia; due to radiation, drugs, or lesions in red bone marrow; largely idiopathic; reduced production of WBC’s, RBC’s, and platelets

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94
Q

types of sideroblastic anemia (x3)

A
  • acquired
  • hereditary
  • reversible
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95
Q

Hemolytic anemia

A

normocytic-normochromic anemia; blood loss anemia; sickle cell

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96
Q

Absolute polycythemia

A

increase in red cell mass caused by increased erythropoiesis; determined by hematocrit

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97
Q

Types of absolute polycythemia (x2)

A
  1. primary

2. secondary

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98
Q

Primary polycythemia (polycythemia vera)

A

genetic; body is producing too many RBC’s and bone marrow produces high number of WBC’s and platelets

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99
Q

manifestations of primary polycythemia

A
  • splenomegaly (spleen ridding of excess cells)
  • thick blood, risk for clotting
  • high BP
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100
Q

Risk factors for primary polycythemia

A

white
male
55-80 y/o

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101
Q

Treatment of polycythemia

A

bleed the patient and give anticoagulants; with no treatment, 50% of pt’s die in 18 months

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102
Q

Causes of secondary polycythemia

A
  • emphysema
  • chronic bronchitis
  • renal failure
  • high altitude
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103
Q

SEcondary polycythemia

A

occurring as a physiologic response to tissue hypoxia

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104
Q

Types of alterations of leukocyte function (x7)

A
  1. quantitative
  2. granulocyte
  3. agranulocyte
  4. infectious mononucleosis
  5. leukemia
  6. malignant lymphoma
  7. multiple myeloma
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105
Q

Leukocytosis

A

quantitative alteration to leukocytes; high levels of WBC’s; normal is 7400

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106
Q

causes of leukocytosis

A
  • infection
  • strenuous exercise
  • emotions
  • anesthesia exposure
  • extremes in temperature
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107
Q

leukopenia

A

low levels of WBC’s, below 6000.

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108
Q

Causes of leukopenia

A
  • radiation of bone marrow
  • autoimmune disease
  • immunodeficiency
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109
Q

granulocytosis

A

abnormally large number of granulocytes in blood or tissues.

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110
Q

neutrophilia

A

granulocyte alteration; high levels of neutrophils

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111
Q

shift to the left

A

granulocyte alteration; WBC’s ar ebeing used up so much that the bone marrow is releasing a lot of immature cells

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112
Q

shift to the right

A

granulocyte alteration; once infection is under control, return to normal, so number of immature WBC’s go down

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113
Q

neutropenia

A

granulocyte alteration; abnormally low level of neutrophils

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114
Q

agranulocytosis

A

granulocyte alteration; absence or severely low level of WBC’s

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115
Q

Eosinophilia

A

granulocyte alteration; higher than normal amount of eosinophils

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116
Q

Eosinopenia

A

granulocyte alteration; lower than normal amount of eosinophils

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117
Q

basophilia

A

granuloygranulocyte alteration; higher than normal amount of basophils

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118
Q

basopenia

A

granulocyte alteration; lower than normal amount of basophils

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119
Q

monocytosis

A

agranulocyte alteration; increased number of monocytes in the blood

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120
Q

monocytopenia

A

agranulocyte alteration; lower number of monocytes in the blood

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121
Q

lymphocytosis

A

agranulocyte alteration; higher than normal number of lymphocytes in the blood

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122
Q

lymphocytopenia

A

agranulocyte alteration; lower than normal amount of lymphocytes in the blood

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123
Q

Infectious mononucleosis (IM)

A

alteration of leukocyte function; acute infection of B lymphocytes with Epstein Barr Virus; “kissing disease”

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124
Q

Manifestations of IM:

A
  • incubation 30-50 days
  • swelling of cervical lymph nodes
  • splenomegaly
  • sore throat
  • affects y/a between 15-35
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125
Q

leukemia

A

alteration of leukocyte function; malignant disorder of the blood and blood-forming organs, exhibiting an uncontrolled proliferation of dysfunctional leukocytes; named after the type of cell that went rogue

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126
Q

Causes of leukemia:

A
  • Genetic predisposition can alter nuclear DNA of a single cell (abnormal chromosomes, aplastic anemia, down syndrome)
  • acquired disorder that progresses to acute leukemia (polycythemia, Hodgkin lymphoma, ovarian cancer, sideroblastic anemia, large doses of radiation and chemo)
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127
Q

manifestations of leukemia

A

(related to bone marrow depression)

  • fatigue
  • bleeding
  • fever
  • HA
  • vomiting
  • facial palsy
  • blurred vision
  • auditory disturbances (infiltration of neurologic system)
  • bone pain
  • liver, spleen, and lymph node enlargement
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128
Q

Acute leukemia

A

quicker and more deadly; onset sudden; undifferentiated and immature blastic cells; bone pain due to increased pressure from proliferation of cells; enlargement of spleen, liver, lymph nodes

129
Q

Types of Acute leukemia (x2)

A
  1. ALL (acute lymphocytic leukemia)

2. AML (myelogenous)

130
Q

Acute lymphocytic leukemia (ALL)

A

85% B lymphocytes line; least common cause of all types of leukemia

  • most common cancer in children
  • chemotherapy cures 65% adults, 85% kids
131
Q

Acute myelogenous Leukemia (AML)

A
  • adolescent or 55

- 20% 5 year survival rate

132
Q

Chronic leukemia

A

onset insidious, more differentiated cells and readily identified, most cases in adults

133
Q

Types of chronic leukemia (x2)

A
  1. chronic lymphocytic leukemia (CLL)

2. Chronic myelogenous leukemia (CML)

134
Q

chronic lymphocytic leukemia (CLL)

A

most often B cell transformation

  • 50-70
  • 73% survival
  • treat only if symptomatic
135
Q

chronic myelogenous leukemia (CML)

A

not very common

  • 30-50
  • 95% have Philadelphia chromosome
  • frequently enters accelerated phase with poor prognosis
  • allogenic bone marrow transplant increases survival rates 20-30%
136
Q

Philadelphia chromosome

A

translocation of chromosomes 9 and 22

137
Q

Malignant lymphomas

A

alterations of leukocyte function; tumors of

  • primary lymphoid tissue or the thymus and bone marrow
  • secondary lymphoid tissue or lymph nodes, spleen, tonsils, and intestinal lymphoid tissue
138
Q

Types of malignant lymphomas (x2)

A
  1. Hodgkin’s disease

2. Non-hodgkin’s lymphoma

139
Q

Hodgkin’s disease

A

malignant lymphoma; REED-STERNBERG CELLS (malignant transformation of lymph cells); bi/-multi-nucleate

140
Q

Pathophysiology of Hodgkin’s disease

A

progression from one group of lymph nodes to another

141
Q

Manifestations of Hodgkin’s disease (due to rapid proliferation of abnormal lymphocytes)

A
  • enlarged painless lymph nodes in neck
  • cervical, axillary, inguinal and retroperitoneal lymph nodes commonly affected=lymphadenopathy
  • systemic symptoms: fever, night sweats, pruritis, weakness, weight loss
142
Q

Diagnosis of Hodgkin’s disease

A

Staging (Cotswold)

143
Q

Etiology of Hodgkin’s disease

A

unknown; derived from B lymphocyte that would normally induce to undergo apoptosis

144
Q

Treatment of Hodgkin’s disease

A

Stages I & II: excision and radiation
Stages III & IV: add chemo
-75% cure rate

145
Q

Non-Hodgkin’s lymphomas

A

malignant lymphoma; includes a variety of lymphomas including myelomas that originate from B cells at various stages of differentiation, T-cell, NK cell neoplasms;
DO NOT HAVE REED-STERNBERG CELLS

146
Q

Risk factors for Non-Hodgkin’s lymphoma

A
  • family hx
  • exposure to a variety of mutagenic chemicals
  • irradiation
  • infection with cancer-related viruses (EBV, HIV, Hep C)
147
Q

Manifestations of Non-Hodgkin’s lymphoma

A
  • enlarged painless lymph nodes in neck
  • cervical, axillary, inguinal and retroperitoneal lymph nodes commonly affected=lymphadenopathy
  • systemic symptoms: fever, night sweats, pruritis, weakness, weight loss
  • pleural effusion
  • abdominal pain
  • splenomegaly
  • joint symptoms
148
Q

treatment of Non-Hodgkin’s lymphoma

A
  • radiation and chemo
  • bone marrow transplant
  • harder to treat due to lack of ability to determine where exactly it is
  • 1 year-77% cure
  • 5 year-59%
  • 10 year-42%
  • nodular lymphoma has better prognosis than diffuse disease
149
Q

Multiple myeloma

A

alteration of leukocyte function; B cell cancer arising from a malignant plasma cell that infiltrates and destroys bone marrow

150
Q

pathophysiology of multiple myeloma

A

involved chromosomal translocations which recur

151
Q

manifestations of multiple myeloma

A
  • elevated calcium
  • renal failure
  • anemia
  • bone lesions leading to fractures
  • proteinuria
  • peak age of incidence is 65 y/o
152
Q

treatment of multiple myeloma

A
  • chemo
  • radiation
  • plasmapheresis
  • stem cell transplantation
  • bone marrow transplant
  • survival usually less than 3 years
153
Q

Disorders of platelet function (x2)

A
  • Thrombocytopenia

- Thrombocythemia

154
Q

Thrombocytopenia

A

disorder of platelet function; reduced platelet production, increased consumption, or both (140,000-300,000 is normal); risk for hemorrhage is at 50,000; may result in 3 mechanisms

155
Q

What are the 3 mechanisms of Thrombocytopenia?

A
  1. heparin-induced thrombocytopenia (HIT)
  2. Idiopathic (Immune) thrombocytopenic purpura (ITP)
  3. Thrombotic thrombocytopenia purpura
156
Q

Heparin-induced thrombocytopenia (HIT)

A

disorder of platelet function-thrombocytopenia; immune response to heparin, make IgG antibodies and ends up decreasing the platelet counts; bruising, petichiae

157
Q

Idiopathic (Immune) thrombocytopenic purpura (ITP)

A

disorder of platelet function-thrombocytopenia; make antibodies to our platelets; can be acute or chronic; make IgG antibodies that cause damage to the platelets

158
Q

Thrombotic thrombocytopenia purpura

A

disorder of platelet function-thrombocytopenia; platelets aggregate and occlude tiny vessels, so they are used up

159
Q

Thrombocythemia

A

disorder of platelet function;

  • Essential (primary): levels above 400,000. Excessive clotting; can be essential or can happen secondarily after splenectomy. Must have vitamin K and calcium for clotting
  • Secondary
160
Q

Disorders of coagulation

A

Usually due to defects or deficiencies of one or more clotting factor

161
Q

Hereditary disorders of impaired synthesis of coagulation factors

A
  • Hemophilia A

- Von Willebrand Disease

162
Q

Hemophilia A

A

hereditary disorder of impaired synthesis of coagulation factor; Deficient in single factor, factor VIII; hereditary; passed from mother to son

163
Q

Von Willebrand Disease

A

Hereditary disorders of impaired synthesis of coagulation factors; caused by multiple clotting factor deficiencies

164
Q

Impaired synthesis of coagulation factors due to impaired homeostasis (x2)

A
  • Deficiency of Vitamin K

- Liver Disease

165
Q

Consumptive thrombohemorrhagic disorders-DIC

A

clotting and hemorrhage occur within the vascular system simultaneously; complication from someone else’s blood

166
Q

Conditions associated with DIC

A
  • Malignancies
  • Infection
  • trauma
  • pregnancy complications
  • liver disease
167
Q

Treatment of DIC

A
  • Manage primary disease-eliminate underlying pathology
  • control ongoing thrombosis (e.g. heparin use)
  • maintain organ function-adequat fluid replacement to ensure adequate circulating blood volume to maintain perfusion
168
Q

Manifestations of DIC

A

Bruising all over body; small areas of clots

169
Q

Thromboembolic disorders

A

disorders from thrombus or embolus

170
Q

Thrombus

A

fixed clot

171
Q

embolus

A

moving clot

172
Q

What can happen if a clot obstructs blood flow to the heart, brain, or lungs?

A

death

173
Q

What does hypercoagulability cause with thromboembolic disorders?

A

deficiency in anticoagulation proteins

174
Q

Treatment of thromboembolic disorders

A
  • parenteral heparin
  • oral coumadin
  • streptokinase/urokinase
175
Q

Risk factors for spontaneous thrombi

A

Virchow triad

176
Q

Virchow triad

A

Group of risk factors for clot formation:

  • loss of integrity of vessel wall
  • abnormalities of blood flow
  • alterations in blood constituents (hyper coagulability)
177
Q

Path of blood through the heart:

A

http://www.dummies.com/how-to/content/the-path-of-blood-through-the-human-body.html

178
Q

Varicose veins

A

veins in which blood has pooled resulting in vessels that are distended, tortuous, and palpable

179
Q

Varicose veins in legs are caused by…

A

trauma to the saphenous vein that damages one or more valves and permits backflow; surrounding tissue becomes edematous because of increased hydrostatic pressure

180
Q

Standing for long periods of time can cause…

A

varicose veins in the legs (gravity)

181
Q

Chronic Venous Insufficiency (CVI) is caused by…

A

pooling of blood in veins of the lower extremities

182
Q

Chronic Venous Insufficiency (CVI) effects:

A
  • hyperpigmentation of the skin over the feet and ankles

- edema that may progress to the knees

183
Q

Venous stasis ulcers are caused by…

A

trauma or pressure that lowers oxygen supply by further reducing blood flow into the area (cell death and necrotic tissue develop)

184
Q

Venous thrombi are more common than arterial thrombi due to…

A

lower BP and flow in veins

185
Q

Risk factors for venous thrombi

A
  • increased age
  • long-term bed rest
  • genetic abnormalities (increased state of hyper coagulability)
186
Q

Manifestations of DVT

A
  • extreme tenderness
  • swelling
  • redness in area of thrombus
  • skin discoloration
  • edema
  • pain at site
187
Q

Risk factors for Deep Vein Thrombosis (DVT)

A
  • conditions that predispose to blood flow stasis
  • endothelial injury
  • hypercoagulability
188
Q

Treatments for varicose veins and chromic venous insufficiency

A
  • compression stockings
  • exercise
  • strip saphenous veins
189
Q

Superior vena cava syndrome (SVCS)

A

progressive occlusion of SVC that leads to venous distention in the upper extremities and head

190
Q

Causes of Superior Vena Cava Syndrome

A

bronchogenic cancer*
lymphomas
metastasis of other cancers

191
Q

Manifestations of Superior Vena Cava Syndrome

A

-Headache
-visual disturbances
-impaired consciousness
-respiratory distress
(most due to edema)

192
Q

Hypertension

A

systolic pressure exceeds 140 mmHg and diastolic exceeds 90 mmHg

193
Q

causes of hypertension

A

Increased cardiac output, total peripheral resistance or both.

194
Q

causes of primary hypertension

A

combination of genetic and environmental

195
Q

Risk factors for hypertension

A 
family history
advancing age
gender
high sodium intake
glucose intolerance
cigarette smoking
obesity
heavy alcohol consumption
low dietary potassium
calcium
magnesium
196
Q

causes of secondary hypertension

A
  • systemic disease process that raises peripheral vascular resistance or cardiac output
  • renal disease
  • adrenal disorders
  • vascular disease
  • drugs
197
Q

manifestations of secondary hypertension

A
  • sudden onset
  • pressure often higher than primary hypertension
  • BP can return to normal if cause is removed
198
Q

causes of Isolated systolic hypertension (ISH)

A

-rigidity of aorta due to calcification of fibers

199
Q

manifestations of isolated systolic hypertension

A
  • systolic BP above 140 but diastolic BP below 90
  • seen in 65+
  • cardio and CV events
200
Q

Complicated hypertension-sustained primary hypertension

A
  • causes pathological effects, demodynamic alterations, and fluid and electrolyte imbalances
  • compromises the structure and function of vessels, heart, kidneys, eyes, and brain
  • LV hypertrophy
  • angina pectoris
  • CHF
  • CAD
  • MI
  • Sudden death
201
Q

Malignant hypertension

A

rapid progressive hypertension in which diastolic pressure is usually above 140 mmHg

202
Q

Manifestations of malignant hypertension

A
  • profound cerebral edema that disrupts cerebral function
  • no symptoms early (“silent disease”)
  • signs and symptoms related to organs affected
203
Q

Treatment of malignant hypertension

A

Managed by medication and nonpharmacological methods

  • reduce risk factors (e.g., smoking, alcohol use)
  • diuretics
  • Beta blockers
204
Q

orthostatic hypotension

A

drop in both systolic and diastolic arterial BP on standing from a reclining position

205
Q

Manifestations of orthostatic hypotension

A
  • vasodilation
  • blood pooling
  • sluggish response
206
Q

chronic orthostatic hypotension

A

may be secondary to disease or primary/idiopathic (men more prone than women, older more than younger adults)

207
Q

Aneurysm

A

localized dilation or outpouching of a vessel wall or cardiac chamber

208
Q

Causes of aneurysm

A

atherosclerosis
hypertension
congenital weakness

209
Q

True aneurysm

A

involve all 3 layers of arterial wall; weakening of wall

210
Q

fusiform circumferential

A

most common form of true aneurysm

211
Q

fusiform saccular

A

outpouching at one side of the wall

212
Q

3/4 of all of these occur in abdominal aorta

A

aneurysms

213
Q

False aneurysm

A

extravascular hematoma that communicates with intravascular space; usually from trauma

214
Q

aortic dissection

A

tear in the intima and blood enters the wall of the artery

215
Q

manifestations of aneurysm

A
  • asymptomatic until rupture
  • dysphagia
  • dyspnea
  • ischemia
  • increased cranial pressure (circle of Willis)
216
Q

treatment of aneurysm

A

surgical*

clot-stabilizing drugs if leaking cerebral aneurysm

217
Q

What are Raynaud’s Disease and Phenomenon (Peripheral Vascular Disease)?

A

Attacks of vasospasm in the small arteries and arterioles of the fingers and, less commonly, the toes

218
Q

What is Raynaud’s phenomenon caused by?

A

A secondary phenomenon to systemic diseases such as collagen vascular disease, pulmonary hypertension, myxedema trauma, serum sickness, or long-term exposure to cold or vibrating machinery

219
Q

What is Raynaud’s disease caused by?

A

Unknown origin, but is a primary vasospastic disorder affecting young women with genetic predisposition
-Triggered by cold, emotional stress, and cigarette smoking that stimulate sympathetic NS

220
Q

Manifestations of Raynaud’s disease/phenomenon

A
  • Changes in color of skin
  • numbness
  • sensation of cold in the digits
  • Rubor: as blood flow returns
  • Throbbing: as blood flow returns
  • Parasthesia: as blood flow returns
  • severe ischemia can eventually cause ulceration and gangrene
221
Q

Treatment of Raynaud’s phenomenon

A

remove stimulus or treat primary disease causing this phenomenon

222
Q

Treatment of Raynaud’s disease

A

-prevention or alleviation of vasospasm by reducing exposure to cold, emotional stress, and cigarette smoking

223
Q

Arteriosclerosis

A

chronic disease of the arterial system characterized by abnormal thickening and hardening of the vessel walls

224
Q

Pathophysiology of arteriosclerosis

A

smooth muscle cells and collagen fibers migrate into the tunica intima, causing it to stiffen and thicken, decreasing lumen size
*happens as a normal part of aging

225
Q

Atherosclerosis

A

most common form of arteriosclerosis in which the thickening of vessel walls is caused by hardening of soft deposits of intra-arterial fat and fibrin
*may take several forms based on vessel location, age, genetic and physiologic status, risk factors

226
Q

Atherogenesis

A

Begins with injury to the endothelial cells of arteries due to smoking, etc.

227
Q

Pathophysiology of atherogenesis

A
  • injured cells unable to produce normal amounts of antithrombic and vasodilating cytokines
  • macrophages oxidize LDL to produce foam cells which form fatty streaks (flat, yellow, lipid-filled smooth muscle cell)
  • fibrous plaque forms (lesion of advancing atherosclerosis consisting of lipid laden smooth muscle cells surrounded by collagen, elastic fibers, and mucoprotein matrix; protrudes into lumen, invades tunica intima and possible muscular tunica media, and if it progresses sufficiently occludes the arterial lumen)
  • complicated lesion (fibrous plaque altered by hemorrhage, calcification, cellular necrosis, and blood clots throughout the intimal layer; altered structure becomes rigid and causes extensive vascular occlusion)
228
Q

Clinical manifestations of atherosclerosis

A
  • High BP
  • Cerebral or Myocardial ischemia (life threatening)
  • all result from inadequate tissue perfusion
229
Q

Management of atherosclerosis

A
  • removal of initial causes of vessel injury and preventing lesion progression
  • aspirin or other non-clotting drugs may be used
  • Exercise, smoking cessation, control of hypertension and diabetes
  • Reduce fat intake to less than 30%, cholesterol intake reduced to 250-300mg
230
Q

What happens in Coronary Artery Disease (CAD)?

A
  • diminished myocardial blood supply until deprivation impairs myocardial metabolism
  • persistent ischemia causes acute coronary syndromes including infarction or death
  • CAD is responsible for 1/3 of all U.S. deaths
231
Q

Non-modifiable risk factors for Coronary Artery Disease (CAD)

A
  • genetic predisposition
  • advanced age
  • male gender
  • postmenopausal women (estrogen protects us)
232
Q

Modifiable risk factors for Coronary Artery Disease (CAD)

A
  • dyslipidemia
  • hypertension
  • cigarette smoking/secondhand smoke
  • insulin diabetes and resistance
  • obesity (65% of U.S. is obese)
  • sedentary lifestyle
233
Q

What is dyslipidemia?

A

abnormal concentrations of serum lipoproteins (1/2 of U.S. population has this)

234
Q

Myocardial Ischemia

A

narrowing of a major coronary artery by more than 50% impairs blood flow enough to hamper cellular metabolism
*most common cause is atherosclerosis

235
Q

How does supply/demand work in myocardial ischemia?

A

There is an imbalance between coronary blood supply and myocardial demand

  • supply is reduced by increased resistance in coronary vessels, hypotension, decreased blood volume, valvular incompetence, anemia
  • demand is increased by high SBP, increased ventricular volume, LV hypertrophy, increased HR, hyperviscosity
236
Q

Manifestations of reversible myocardial ischemia

A
  • stable angina pectoris
  • Prinzmetal angina
  • Silent ischemia
  • Mental stress
237
Q

Stable angina pectoris

A

manifestation of reversible myocardial ischemia

  • “choked chest”
  • increased work demands of the heart are not met by increased blood flow to the heart
  • mistaken for indigestions
  • may take a vasodilator (ex: nitroglycerin)
238
Q

Prinzmetal angina

A

chest pain that occurs unpredictably and at rest or with minimal exercise
manifestation of reversible myocardial ischemia
-“variant angina”
-result of vasospasms of cardiac arteries
*may be helped with calcium channel blockers
*may be helped with nitrates

239
Q

Silent ischemia

A

manifestation of reversible myocardial ischemia

  • absence of angina pain
  • may be asymptomatic, or patient may complain of feeling a little “off”
  • more often in women
  • may be in people with high threshold for pain
  • may be in people with neuropathy that cannot sense pain
240
Q

Mental stress

A

manifestation of reversible myocardial ischemia

  • induced ischemia
  • person does not experience angina even though the artery is occluded
  • increase in BP and myocardial oxygen demand
  • can result in ischemia that may lead to MI
241
Q

Treatment of myocardial ischemia

A
  • percutaneous coronary intervention (PCI)

- coronary artery bypass graft (CABG)

242
Q

Percutaneous coronary intervention (PCI)

A

narrowed coronary vessels are dilated with a catheter (may include placement of coronary stent)

243
Q

Coronary artery bypass graft (CABG)

A

using saphenous vein to replace injured tissue

244
Q

Acute Coronary Syndrome

A

sudden coronary obstruction by thrombus over a ruptured atherosclerotic plaque

245
Q

Unstable angina

A

Acute Coronary Syndrome

  • signals that atherosclerosis plaque has become complicated and infarction may soon follow
  • superficial erosion of plaque leads to transient episodes of thrombotic vessel occlusion and vasoconstriction
  • new onset angina, angina at rest, angina of increasing severity
  • ST-segment depression and T wave inversion
  • 20% proceed to MI
246
Q

Myocardial Infarction (MI)

A

Acute Coronary Syndrome

  • prolonged ischemia (lack of oxygen for >20min causing irreversible damage to heart muscle)
  • CPK-MB enzyme released (enzyme specific to heart muscle)
247
Q

Structural/functional changes in MI

A
  • myocardial stunning
  • hibernating myocardium
  • myocardial remodeling
248
Q

myocardial stunning

A

Change during MI

-temporary loss of muscle function

249
Q

hibernating myocardium

A

change during MI

-goes through metabolic adaptation to prolong the survival of the myocardium

250
Q

myocardial remodeling

A

change during MI

-myocardium hypertrophies and loses contractile function on the side distant to the side of infarction

251
Q

clinical manifestations of MI

A
  • sudden severe chest pain-heavy and crushing
  • radiation of pain to neck, jaw, back, shoulder, or left arm
  • elderly or those with diabetes have “silent” infarction
  • N &V may occur
  • diaphoresis, cool clammy skin
252
Q

Serum markers of MI

A
  • Troponin complex-most significant indicators of MI, especially I and T components
  • MB fraction (membrane bound faction)
  • lactate dehydrogenase (LDH)-elevates but maxes after 72 hrs
  • creatinine kinase (CK)
253
Q

Disorders of the pericardium

A
  • acute pericarditis
  • pericardial effusion
  • constrictive pericarditis
254
Q

acute pericarditis

A
  • Cause: 90% due to viruses or are idiopathic
  • creates a friction rub
  • severe pain that gets worse as person breathes
  • worse laying down
  • Tx: antiinflammitory drugs
255
Q

pericardial effusion

A

Excess fluid in the pericardial cavity surrounds and presses on heart wall which interferes with expansion of the heart, decreased amount o blood to the lungs, decreased output back to the heart, and a decreased amount sent to the body
-Tamponade

256
Q

Tamponade

A

as a result of pressure, this interferes with right atrial filling during diastole
-may need to be treated with pericardial centesis to remove fluid

257
Q

constrictive pericarditis

A

Causes: exposure to radiation, RA, cabbage surgery

  • pericardium becomes fibrotic
  • scarring resulting from effusion of visceral and parietal layers of pericardium encases pericardium in a hard shell which decreases cardiac output ability
258
Q

Disorders of the myocardium (cardiomyopathies)

A
  • dilated
  • hypertrophic
  • restrictive
259
Q

dilated myocardium

A

most common cardiomyopathy

  • most idiopathic
  • most result in dilated LV
  • Some result from CHF
  • contractility of ventricle is reduced which reduces cardiac output
  • death of 20-50% in one year
260
Q

hypertrophic myocardium

A

wall of ventricle becomes very thick, less space for blood in ventricle

  • atrium may become diluted
  • mostly effects diastolic function: wall cannot relax so it increases the diastolic pressure
261
Q

restrictive myocardium

A

least common cardiomyopathy

  • often results from scleroderma
  • compliance of sclera is reduced so the blood backs up into the ventricle… atrium may end up dilated
262
Q

Valvular dysfunction

A

valves do not open or close properly

  • Stenosis
  • Regurgitation
  • Prolapse
263
Q

Types of valvular stenosis

A
  • aortic valve stenosis

- mitral valve stenosis

264
Q

Types of valvular regurgitation

A
  • aortic valve regurg
  • mitral valve regurg
  • tricuspic valve regurg
265
Q

Stenosis is…

A

narrowing of the valve so it does not open properly; increases workload on chamber prior to the valve trying to force blood through the narrow opening; may result in hypertrophyy of that chamber

266
Q

Regurgitation is…

A

distortion of the valve so it does not close properly allows back flow, increases amount of blood that must be pumped and increases cardiac workload
-chamber may dilate to accommodate increased workload

267
Q

Mitral valve prolapsed syndrome

A

Mitral valve becomes floppy and leaflets bulge into LA during systole

  • seen more often in women
  • many times asymptomatic
  • may have chest pain, dyspnea, fatigue, lightheadedness
  • occurs through autosomal dominance inheritance
  • may manage through decreasing caffeine intake, stop smoking, and stop alcohol use
268
Q

aortic valve stenosis

A

LV is unable to pump out all the blood so it decreases stroke volume of LV

  • Causes: rheumatic fever or congenital malformation
  • S&S: drop in systolic BP, angina, fainting, SOB
  • May end up with LV hypertrophy
269
Q

mitral valve stenosis

A

blood cannot leave the LA so it increases pressure and the LA becomes dilated

  • blood backs up to the lungs and causing pulmonary congestion
  • may experience diastolic murmur
  • Cause: rheumatic fever
270
Q

Aortic valve regurgitation

A

AV does not close completely so during diastole blood flows back tot he LV causing it to dilate due to volume overload

  • Cause: rheumatic fever or improperly functioning prosthetic valve
  • S&S: heart pounding out of chest; hyperkinetic/”water hammer” pulse
271
Q

mitral valve regurgitation

A

when LV contracts, some of the blood backflows into the LA instead of the AV during systole, so this causes a systolic murmur

  • blood may backflow into the lungs resulting in CHF
  • LV may wear out as a result of increased force
272
Q

tricuspid valve regurgitation

A
  • much more common than stenosis
  • usually associated with failure and dilation of RB since blood is backflowing into the RV
  • may cause pulmonary hypertension, edema, asciites
273
Q

dysrhythmias

A

caused by an abnormal rate of impulse generation or an abnormal conduction of impulses

  • sinus bradycardia
  • sinus tachycardia
  • sinus dysrhythmia
  • premature atrial contraction
  • ventricular tachycardia
  • ventricular fibrillation
  • heart block
274
Q

sinus bradycardia

A

dysrhythmia
slow HR of less than 60 bpm
*may be normal in athletes or during sleep

275
Q

sinus tachycardia

A

dysrhythmia
fast HR of greater than 100 bpm
-can indicate heart failure, hyperthyroidism, compensating for a decrease in blood volume
*normal response when exercising, in fever

276
Q

sinus dysrhythmia

A

dysrhythmia
gradually lengthening and shortening of periods between QRS complex
*can be normal when sleeping

277
Q

Premature atrial contraction (PAC)

A

dysrhythmia
disconnect between atria contracting and the rest of the process of moving the blood through the heart
-Cause: stress, tobacco smoking, caffeine
*may or may not cause an issue

278
Q

Premature ventricular contraction (PVC)

A

dysrhythmia

cells depolarize and trigger a spontaneous contraction

279
Q

ventricular tachycardia

A

dysrhythmia
ventricular rate of 70-100 bpm
-reduces filling of ventricle during diastole=decreased cardiac ouput or perfusion
*may be life-threatening/progress to V-fib

280
Q

Ventricular fibrillation

A

dysrhythmia
ventricle is quivering but not contracting so no cardiac output or perfusion
-defibrillation necessary to stop this and let SA node take over

281
Q

heart block

A

dysrhythmia
impulse is impaired going from atria to ventricle
-can result in increasing PR interval or may result in delaying impulse enough that the atria beats again
-sometimes will miss a ventricular contraction
-3rd degree
-Tx: independent pace makers

282
Q

Pathophysiology of heart failure

A

failure of heart to work as a pump due to many different causes

283
Q

compensatory mechanisms of heart failure

A

put into place because cells of the body are not getting enough oxygen-good for short term but not intended for long term use becasue they can damage other parts of the body

  • increase SNS activity
  • renin-angiotensin mechanism
  • natriuretic peptides
  • endothelin
  • myocardial hypertrophy
284
Q

Increase SNS activity

A

compensatory mechanism of heart failure

  • activated in response to decrease in cardiac output
  • stimulates peripheral vasoconstriction to incraese HR to get blood to heart
  • increased blood glucose
  • decreased blood flow to kidneys
285
Q

Renin-angiotensin mechanism

A

compensatory mechanism of heart failure

  • renin reduced due to decreased blood flow to kidney
  • BP increases due to fluid retention, aldosterone released
  • sodium and water are saved and potassium is secreted in urine
286
Q

natriuretic peptides

A

compensatory mechanism of heart failure

  • high in individuals with heart failure
  • released in response to increased stretch receptors
287
Q

endothelin

A

compensatory mechanism of heart failure

  • released from endothelial cells
  • potent vasoconstrictors
288
Q

myocardial hypertrophy

A

compensatory mechanism of heart failure

  • due to increased work load and increased systolic function of the heart
  • more blood flow needed in heart if it gets bigger
289
Q

Etiology of Left heart failure (congestive)

A

MI
cardiomyopathy
stenosis/regurg at aortic SLV

290
Q

pathophysiology of left heart failure

A

results in pulmonary edema (often at night after person has been reclining for some time)

291
Q

S&S of left heart failure

A
  • fluid retention and edema
  • respiratory manifestations (rales, cough, orthopnea, dyspnea)
  • decreased urinary output
  • cachexia and malnutrition
  • cyanosis
292
Q

Etiology of right heart failure

A

stenosis/regurg at tricuspid or PSLV

  • RV infarction
  • cardiomyopathy
  • Congestive HF
  • acute or chronic pulmonary disease
293
Q

S&S of right heart failure

A
  • asciites
  • GI disorder
  • liver and spleen engorgement
  • distended jugular veins
  • dependent edema
294
Q

high-ouput failure

A

inability of the heart to supply the body with nutrients despite adequate blood volume and normal myocardial contractility

295
Q

S&S of high-output failure

A
  • anemia
  • septicemia
  • hyperthyroidism
  • beriberi
296
Q

Shock

A

occurs when cardio system fails to perfuse adequately and can result in multiple organ failure

297
Q

Shock is due to…

A

1) impairment of oxygen use

2) impairment of glucose use

298
Q

Types of shock

A
  • cardiogenic
  • hypovolemic
  • neurogenic
  • anaphylactic
  • septic
299
Q

cardiogenic shock

A

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

300
Q

etiology of cardiogenic shock

A 
MI
myocardia ischemia
CHF
infection
dysrhythmias
drug toxicity
301
Q

pathophysiology of cardiogenic shock

A

failure of heart to eject blood resulting in hypotension and inadequate cardiac output

302
Q

manifestations of cardiogenic shock

A
  • extreme heart failure
  • pulmonary edema
  • 70% mortality rate
303
Q

treatment of cardiogenic shock

A

increase cardiac output but decrease workload

  • vasodilators
  • thrombolytics
  • angioplasty
  • elevate head and shoulders as a quick fix
304
Q

etiology of hypovolemic shock

A

loss of blood bolume due to loss of whole blood/plasma

-begins when volume lost is at least 15%

305
Q

compensatory mechanisms of hypovolemic shock

A

increase HR and vascular resistance to increase cardiac output and tissue perfusion
-renin-angiotensin mechanism

306
Q

Manifestations of hypovolemic shock

A

high SVR, poor skin turgor, thirst, oliguria, rapid HR, thready pulse, decreased mental status

307
Q

treatment of hypovolemic shock

A

fluid replacement and ADH

308
Q

neurogenic shock

A

result of widespread and massive vasodilation that results from PSNS overstimulation and SNS understimulation

309
Q

etiology of neurogenic shock

A

spinal cord injuries

310
Q

etiology of anaphylactic shock

A

hypersensitivity reaction (Type I)

311
Q

S&S of anaphylactic shock

A

vasodilation, peripheral pooling, heat, redness (inflammation)

312
Q

treatment of anaphylactic shock

A

epinephrine

313
Q

septic shock

A

result of infection/presence of bacteria in blood (bacteremia)

314
Q

treatment of septic shock

A
  • catheter
  • broad spectrum antibiotics
  • remove infection
  • IV fluids
  • careful monitoring
  • corticosteroids
  • vasopressin
  • insulin
  • nutrition
  • prevent DVT and ulcers
315
Q

manifestations of septic shock

A

skin warm and flushed; 40% mortality

316
Q

complications of shock

A
  • acute respiratory distress syndrome
  • acute renal failue
  • GI complications
  • DIC
  • Multiple Organ Dysfunction syndrome
317
Q

pathophysiology of right heart failure

A
  • left heart failure
  • COPD
  • cystic fibrosis
  • acute respiratory distress syndrome
318
Q

multiple organ dysfunction syndrome (MODS)

A

progressive dysfunction of 2+ organ systems resulting from uncontrolled inflammatory response to a severe illness/injury

319
Q

If you throw a cat out a car window, does it become kitty litter?

A

Message me! You get a special surprise! And I promise it won’t be bubbles or a stress ball.

Pathophysiology (2 decks)

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