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Pathophysiology > Patho Unit 6 > Flashcards

Patho Unit 6 Flashcards

Understand: - Alterations of Hormonal Regulation (Ch 18) - Stress and Disease (Ch 8) - Alterations of Cardiovascular Function (Ch 23) - Alterations of Cardiovascular Function in Children (Ch 24)

1
Q

Hormones

A

Mediator molecules secreted directly into the blood by endocrine glands

  • Receptors are located on the plasma membrane or in the intracellular compartment of a target cell
  • Operate by negative or positive feedback
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2
Q

The Endocrine System

A
  • Pituitary gland
  • Thyroid gland
  • Parathyroid gland
  • Adrenal gland
  • Pineal gland
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3
Q

Other Organs and Tissues that secrete hormones

A
  • Hypothalamus
  • Thymus
  • Pancreas
  • Gonads
  • Kidneys
  • Stomach
  • Liver
  • Small Intestines
  • Skin
  • Heart
  • Placenta
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4
Q

Action of Hormones

A
  • Control the composition of the volume of the INTERNAL ENVIRONMENT
  • Emergency control during physical and mental STRESS
  • Integration of GROWTH and development
  • REPRODUCTIVE control
  • Regulate METABOLISM and energy balance (glucose availability and metabolic rates)
  • Bind to specific protein or glycoprotein receptors on their target cells
  • Target cells have the ability to up- or down-regulate receptors
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5
Q

Hypersecretion

A
  • Glandular neoplasms
  • Ectopic hormone release
  • Antibody mimicking hormone
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6
Q

Hyposecretion

A
  • Receptor disorders
  • Inadequate hormone synthesis
  • Degraded or inactivated hormones
  • Blocking antibodies
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7
Q

Hypothalamus

A

The major link between the Nervous System and the Endocrine System
- Receives input from several regions in the brain: Limbic, RAS, Thalamus

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8
Q

Adenohypophysis

A

The ANTERIOR lobe of the Pituitary

- Connected to the Hypothalamus by BLOOD VESSELS

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9
Q

Neurohypophysis

A

The POSTERIOR lobe of the Pituitary

  • Connected to the Hypothalamus by NEUROSECRETORY NEURONS
  • Diseases are rare and are usually related to abnormal ADH secretion
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10
Q

Oxytocin (OT) and Antidiuretic Hormone (ADH)

A
  • Produced by the cell bodies of the neurosecretory neurons in the Hypothalamus
  • Transported down cell axons to the Posterior Pituitary
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11
Q

Oxytocin

A

Childbirth, suckling, and coitus stimulate its release

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12
Q

ADH

A

Dehydration stimulates its release

  • Controls cells at the Distal Collecting Tubule (DCT) of the kidney to prevent secretion of water
  • Increases Aquaporin (H2O channel) production by DCT cells, which facilitates reabsorption of water and decreases plasma osmolality
  • Decreases urine output
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13
Q

Syndrome of Inappropriate ADH

SIADH

A

Occurs when ADH is secreted despite normal or even elevated levels of body water, and without the absence of normal physiologic stimuli (thirst)

  • Results in the inability to excrete excess water in the urine, and reabsorption of water to the point of causing Hypervolemia and Hyponatremia
  • Cellular edema leads to headache and other neurological signs and symptoms
  • The body is retaining water but the urine is inappropriately concentrated
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14
Q

Diabetes Insipidus

A

Caused by the INSUFFICIENT RELEASE OF ADH despite dehydration

  • Free water continues to be eliminated in the urine, even though it is needed in the body
  • Unlike Diabetes Mellitus there is no glucose in the urine
  • 2 types: Neurogenic and Nephrogenic
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15
Q

Diabetes Insipidus

Neurogenic

A

Results from a lesion in the Hypothalamus, Pituitary, or Infundibulum resulting in decreased ADH secretion
- Most common

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16
Q

Diabetes Insipidus

Nephrogenic

A

A state of insensitivity of the renal tubules to ADH

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17
Q

Hormones of the Anterior Pituitary

A
  • Growth Hormone Releasing Hormone (GHRH)
  • Thyrotropin Releasing Hormone (TRH)
  • Corticotropin Releasing Hormone (CRH)
  • Gonadotropic Releasing Hormone (GnRH)
  • Prolactin Releasing Hormone (PRH)
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18
Q

GHRH

A
  • Stimulates the release of Human Growth Hormone (HGH) from the Anterior Pituitary
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19
Q

HGH

A

Stimulates growth of body cells

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20
Q

TRH

A

Stimulates release of Thyroid Stimulating Hormone (TSH) from the Anterior Pituitary

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21
Q

TSH

A

Stimulates Thyroid Gland

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22
Q

CRH

A

Stimulates release of Adrenocorticotropic Hormone (ACTH) from the Anterior Pituitary

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23
Q

ACTH

A

Stimulates Adrenal Cortex

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24
Q

GnRH

A

Stimulates release of Follicle Stimulating Hormone (FSH) or Lutenizing Hormone (LH) from the Anterior Pituitary

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25
Q

FSH

A

Ova/Sperm development and production

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26
Q

LH

A

Causes maturation of uterine lining, testosterone production, and ovulation

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27
Q

PRH

A

Stimulates release of Prolactin (PRL) from the Anterior Pituitary

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28
Q

PRL

A

Causes Lactation of mammary glands

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29
Q

Hypopituitarism

A

Caused by infarction of the gland, removal/destruction of pituitary, space occupying adenomas, aneurysms that cause compression
- Effects depend on the affected hormone

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30
Q

Panhypopituitarism

A

Absence of all hormones from the Anterior Pituitary

- Treatment may consist of replacing HGH, ACTH, TSH, and sex hormones

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31
Q

Pituitary Dwarfism

A

Results from insufficient HGH release during an individual’s growth phase
- Patient has normal face and intelligence, with normal body proportions

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32
Q

Giantism

A

Caused by a Pituitary Adenoma

  • Excess HGH is released during an individual’s growth phase
  • Now fairly rare because of early detection of Adenomas
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33
Q

Acromegaly

A

Excess HGH is release during adulthood

  • Causes enlargement and elongation of the bones of the face jaw, cheeks, and hands
  • The long bones of the extremities are unaffected because the growth plates are closed
  • With bony and soft tissue overgrowth, nerves can be entrapped
  • Patient may demonstrate muscle weakness, foot drop, and sensory changes
  • Increase in the size and function of sebaceous and sweat glands (acne and increased body odor)
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34
Q

Thyroid Gland

A 
Secretes Thyroxine (T4) and Triiodothyronine (T3)
  - Stores a 100 day supply of hormones in sacs that make up most of the gland
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35
Q

Thyroid Hormones

A
  • Regulate Oxygen use
  • Increase Basal Metabolic Rate (BMR)
  • Increase cellular carbohydrate and protein catabolism
  • Increase reactivity of the nervous system
  • Along with HGH, controls tissue growth and development
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36
Q

Hypothyroidism

A

Most common, it can be a primary abnormality or appear secondary to another disorder

  • BMR decreased
  • Sympathetic Response decreased
  • Weight gain
  • Temperature tolerance: cold intolerance, decreased sweating
  • GI function: constipation, decreased appetite
  • Cardiac Function: low output, Bradycardia
  • Respiratory function: Hypoventilation
  • Muscle/tone reflexes decreased
  • Appearance: Myxedematous
  • General behavior: mental retardation (infants), mental and physical sluggishness
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37
Q

Hyperthyroidism

A
  • BMR increased
  • Sympathetic Response increased
  • Weight loss
  • Temperature tolerance: heat intolerance, increased sweating
  • GI function: diarrhea
  • Cardiac Function: increased output, Tachycardia
  • Respiratory function: Dyspnea
  • Muscle/tone reflexes increased
  • Appearance: enlarged thyroid, decreased blinking
  • General behavior: restlessness, irritable, anxiety, wakefulness
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38
Q

Goiter

A

An enlarged Thyroid Gland due to increased demand for Thyroid Hormones, or anything that causes and increase of TSH

  • Can occur in states of Euthyroid, Hypothyroidism, and Hyperthyroidism
  • Common causes include I2 deficiency, viral or genetic disease, puberty, and pregnancy
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39
Q

Graves Disease

A

An autoimmune disorder where antibodies are made against TSH Receptors of Thyroid Cells

  • Antibodies act as TSH Receptor agonists (turn on the production of Thyroxin)
  • Excess Thyroxin secretion leads to Thyrotoxicosis (symptomatic HYPERTHYROIDISM)
  • Signs: diminished body weight, Exophthalmos (bulging eyes) due to periorbital connective deposition
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40
Q

Thyrotoxic Crisis

“Thyroid Storm”

A

A very dangerous worsening of the Thyrotoxic State

  • Rare, but still dangerous
  • Manifests as Hyperthermia, Tachycardia, nausea and vomiting, diarrhea, high-output heart failure, agitation, delirium
  • If untreated, patient can die within 48 hours
  • Treatment: prevent patient from becoming Hyperthyroid in the first place by blocking hormone production or ablating the gland (surgery or radiation)
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41
Q

Hashimoto Disease

A

Autoimmune destruction of the Thyroid Gland

- Primary Hypothyroid abnormality

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42
Q

Secondary causes of Hypothyroidism

A
  • Toxic Thyroiditis from a bacterial infection of the Thyroid
  • Complication of Thyroid surgery
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43
Q

Myxedema

A

A rare but serious form of severe HYPOTHYROIDISM that results from prolonged insufficient Thyroxin during adulthood

  • The “Myxedema” comes from deposition of connective tissue fibers separated by excessive protein and mucopolysaccharides (these bind to water, causing boggy edema)
  • Results in brittle hair, dry skin (decreased perspiration and sebaceous gland secretion), lethargy, low BMR (temp and heart rate), gain weight easily
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44
Q

Myxedema Coma

A

A CNS-Cardiovascular complication of the disease presenting as Hypothermia (no shivering), Hypoventilation, Hypotension, Hypoglycemia, Lactic Acidosis, and deterioration of mental status
- Medical emergency, and if not promptly treated will result in permanent brain damage or death

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45
Q

Congenital Hypothyroidism

Cretinism

A
  • Congenital Hypothyroidism results from inadequate Thyroid Hormone during Intrauterine growth
  • Signs and Symptoms include lethargy, hypothermia, and bradycardia
  • Because Thyroid Hormones effect HGH, patient also has stunted growth, abdominal protrusion and umbilical hernia
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46
Q

Parathyroid Glands

A

Parathyroid Hormone (PTH) is secreted when the plasma Ca++ is low

  • Increases absorption of Ca++ from the GI tract, reabsorption from the kidneys and stimulates the release of Ca++ from bone (Osteoclast activity)
  • Osteoclast activity is a negative feedback with the Osteoblastic activity of Calcitonin (from the Thyroid) and doesn’t involve the Pituitary
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47
Q

Hyperparathyroidism

A

80-85% of cases are caused by Parathyroid Adenomas, but it can also be caused by a compensatory response to Hypocalcemia

Hyperparathyroidism causes:

  • Increased Osteoclast activity
  • Fragile bones with fractures and abnormal curvatures and bone pain
  • High plasma calcium levels can lead to a number of systemic problems
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48
Q

Hypoparathyroidism

A

Commonly caused by damage to the Parathyroid Glands during thyroid surgery

Signs and Symptoms:

  • Tetany (muscle spasms due to low plasma Ca++ which lowers the threshold for nerve signals to muscle contraction)
  • Patients are treated with oral calcium and vitamin D
  • Can cause Hypoplastic Dentin, bone deformation, and basal ganglia calcifications
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49
Q

Diabetes Mellitus

A
  • 2 types: Type I and Type II
  • Signs and symptoms include Polydipsia, Polyuria, and Polyphagia

Diagnosis:

  • More than one fasting glucose level above 126 mg/dl
  • 2-hour glucose tolerance test >200 mg/dl
  • Random blood glucose >200 mg/dl
  • Elevated levels of HbA1c
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50
Q

Diabetes Mellitus

Type I

A

Typically an immune disease of children, with DESTRUCTION OF THE INSULIN PRODUCING β-ISLETS of the pancreas

  • Genetic factor plus a “trigger” of some sort (virus, food, chemical, or drug). The exact mechanism isn’t known
  • As β-cells are gradually destroyed insulin levels fall and blood sugar levels rise
  • Usually diagnosed under 30 years of age
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51
Q

Diabetes Mellitus

Type II

A

Genetic susceptibility is greater than Type I, but it is also triggered by environmental factors such as obesity

  • Usually develops after 45 years of age
  • The biggest problem is INSULIN RESISTANCE at the cellular level
  • Glucose accumulates in the blood but cannot be properly used by cells
  • Almost all associated with metabolic syndrome (Hyperglycemia, Hypertension, Dyslipidemea, truncal obesity)
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52
Q

Glycosylated Hemoglobin

HbA1c

A

Used to measure long term blood glucose control

  • Increased blood glucose plus insulin resistance, over a long period of time, leads to sugar being deposited on hemoglobin A molecules (HbA1c)
  • Should be around 5%
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53
Q

Hypoglycemia and Insulin Shock

A

Blood glucose levels <60 mg/dl, and is related to activation of the sympathetic nervous system, cessation of glucose delivery to the brain, or both

  • Frequent occurrence in diabetics - especially those on insulin
  • Rapid onset
  • Patients are diaphoretic and appear weak, anxious, and confused
  • Treatment includes fast-acting carbohydrate solution (Coke/Orange juice), intravenous infusions of dextrose containing fluids, or an injection of glucagon
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54
Q 
Diabetic Ketoacidosis
(DKA)
A

Due to a complete lack of insulin, Type I diabetics catabolize fatty acids as a source of energy when glucose is unavailable producing Keto acids

  • Nausea, vomiting, comatose, irritable, general diabetic symptoms
  • Dry, hot, flushed skin and mucous membranes
  • Glucose level >300 mg/dl
  • Treatment: insulin, electrolyte and fluid replacement
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55
Q

Hyperosmolar Hyperglycemic Non-Ketotic Syndrome

HHNKS

A

A condition that manifests as extremely elevated blood glucose levels >700 mg/dl, without acidosis

  • Usually comes on slowly, most often in elderly patients with Type II DM
  • Differs from DKA because of the presence of some small amount of insulin, so no Ketosis develops
  • Dehydration can be severe
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56
Q

Acute Complications of DM

A
  • Hypoglycemia
  • Insulin Shock
  • DKA
  • HHNKS
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57
Q

Chronic Complications of DM

A
  • Microvascular Disease
  • Macrovascular Disease
  • Peripheral Neuropathy
  • Infections
  • Retinopathy (blindness; leading cause)
  • Nephropathy (leading cause)
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58
Q

Microvascular Disease in DM

A

A thickening of the capillary basement membrane; leading to decreased perfusion of tissues

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59
Q

Macrovascular Disease in DM

A

Manifests as a 2-4 fold increase in heart disease

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60
Q

Peripheral Neuropathy in DM

A

Results from multiple metabolic, genetic, and environmental factors, with over 60-70% of patients showing some form of nerve damage

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61
Q

Hormones of the Adrenal Cortex

A
  • Glucocorticoids
  • Mineralocorticoids
  • Gonadocorticoids
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62
Q

Glucocorticoids

A
  • CORTISOL regulates metabolism by promoting the breakdown of proteins and fats, and the formation of glucose
  • This raises blood glucose levels and helps the body deal with stress
  • Powerful anti-inflammatory agents and they also possess immune suppressive properties
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63
Q

Cushing Disease/Syndrome

A

EXCESS CORTISOL usually caused by a tumor of the adrenal gland or a tumor causing excess secretion of ACTH

  • Develops from excess EXOGENOUS Glucocorticoids
  • Causes fat redistribution (moon face, buffalo hump, and a hanging abdomen)
  • Patients also exhibit slow wound healing, Hyperglycemia, acne, Osteoporosis, and susceptibility to infections
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64
Q

Mineralocorticoids

A

Aldosterone is the body’s main mineralcordicoid, regulates water and electrolytes (Na+ and K+)
- Conserves Na+ and H2O but promotes the excretion of H+ and K+

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65
Q

Conn Disease

A

Primary Hyperaldosteroneism

  • Results from excessive aldosterone secretion usually as the result of a tumor in the adrenal cortex
  • Kidneys respond by conserving Na+ and H2O while wasting K+
  • Signs and Symptoms: hypertension, and hypokalemia from renal K+ wasting with its attendant neuromuscular irritability (twitching and cramps)
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66
Q

Adrenogenital Syndrome in Women

A

Hypersecretion of weak androgens (DHEA)

- In women DHEA is masculinizing, causing deep voice and increased body hair

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67
Q

Gonadocorticoid Disorders

A

Adrenogenital Syndromes; congenital adrenal hyperplasia

  • Rare, congenital syndromes
  • A group of autosomal recessive conditions that lead to deficiency of an enzyme needed to make Cortisol
  • In an attempt to compensate, the pituitary produces high levels of ACTH, which results in overproduction of certain intermediary Androgens
  • These hormones have Testosterone-like effects on the fetus and child leading to virilization
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68
Q

Virilization in Women

A

The clitoris is enlarged, and may resemble the male penis to the point that the sex of the child is questioned or mistake

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69
Q

Virilization in Men

A

May have enlarged penile size, but the problem may go undetected
- During development the Androgens may lead to early puberty, with a deep voice and increased body hair

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70
Q

Androgenital Syndrome in Men

A

Hypersecretion of estrogens

- In men Estrogens are feminizing, causing development of female secondary sex characteristics

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71
Q

Addison Disease

A

Results from the autoimmune destruction of the adrenal cortex

  • Leads to hyposecretion of Cortisol and Aldosterone
  • Signs and Symptoms: weight loss, Na+ loss and hyponatremia, K+ retention and hyperkalemia, muscle weakness, dehydration, hypotension, and hypoglycemia
72
Q

Adrenal Medulla

A
  • Secretions are part of the sympathetic nervous system
  • Epinephrine and Norepinephrine
  • Innervated by sympathetic preganglionics
  • Acts similar to a sympathetic postganglionic neuron
  • The secretions of the medulla duplicate and prolong the sympathetic response
73
Q

Pheochromocytoma

A

A benign tumor of medullary cells, and is the only common disorder of this part of the Adrenal Medulla

  • Results in increased secretion of high levels of Medullary Catecholamines, producing an exaggerated (and often dangerous) sympathetic response
  • Signs and Symptoms: malignant hypertension, tachycardia, palpitations, and other dysrhythmias, anxiety can sometimes be very severe and disconcerting
74
Q

Stress

A
  • A person experiences stress when a demand exceeds a person’s coping abilities
  • Stress begins with a stimulus that the brain perceives as stressful and in turn promotes adaptational and survival-related physiologic responses
  • These responses can become dysregulated and cause pathophysiology
75
Q

Distress

A

Demand exceeds a person’s coping abilities

76
Q

Stress is and Interaction Between…

A

Individual differences
- Genes, development, experience

Behavioral responses
- Fight or flight, personal behavior: diet, smoking, drinking, exercise

Physiologic response

77
Q

General Adaptation Syndrome Stages

A
  • Alarm stage
  • Resistance (adaptation) stage
  • Exhaustion stage
78
Q

Alarm Stage

A

Activation of the CNS

  • Sympathetic response
  • Norepinephrine
  • Increased cardiac output
  • Increased BP
  • Promote Hyperglycemia
  • Cause vasoconstriction of vessels in skin, viscera, extremities, and kidneys
  • Causes vasodilation of vessels in the heart, skeletal muscles and the smooth muscle of bronchi
79
Q

The Resistance Stage

A

Activation of the Sympathetic Nervous System causes the Hypothalamus to stimulate the Pituitary Gland resulting in:

  • The adrenal cortex increases ACTH release (controls Aldosterone and Cortisol)
  • The adrenal medulla secretes epinephrine and norepinephrine
  • The pituitary gland secretes TSH
  • Increased secretion of HGH
  • Increased release of ADH from posterior pituitary
80
Q

Cortisol

in the Resistance Stage

A
  • Increases protein catabolism, hyperglycemia, promotes gluconeogenesis in liver cells, and delays the healing process
  • Promotes lipolysis in adipose tissue (especially in the extremities), increases gastric secretion, anti-inflammatory effects
  • Althogh there is an increase in antibody formation, there is an overall decrease in the immune response (decline in lymphocytes)
81
Q

TSH

in the Resistance Stage

A

Increased Thyroxin (increased Basal Metabolic Rate)

82
Q

Aldosterone

in the Resistance Stage

A
  • Increases NA+ and water retention

- Increases blood volume and pressure

83
Q

ADH

A
  • Water retention

- Increases blood volume and pressure

84
Q

Exhaustion Stage

A 
With continuous uncompensated stress, disease can result:
Cardiovascular System
  - coronary artery disease
  - hypertension
  - stroke
  - arrhythmias
Muscular System
  - tension headache
  - muscle contractions (spasms)
Connective Tissues
  - rheumatoid arthritis
  - inflammatory diseases of connective tissue
85
Q

Thrombus

A

A clot that forms in a blood vessel and remains attached

  • Can occlude vessels and cause ischemia or infarction of organs
  • Located in veins, systemic and coronary arteries
  • Cause: conditions encourage activation of the coagulation cascade (roughing of vessel wall, stasis or pooling of blood, infectious agents)
86
Q

Thrombophlebitis

A

Thrombi form in veins, with associated inflammation

87
Q

Thrombi of Heart Valves

A

Due to endocardial inflammation or rheumatic fever

88
Q

Embolism

A

Obstruction of a vessel by moving chunk of material

89
Q

Thromboemboli

A

Thrombi which break loose and travel to another site

90
Q

Air Emboli

A

Air bubble from injection, punctured lung, or open vessel

91
Q

Fat Emboli

A
  • Hip replacement surgery

- Broken bone

92
Q

Pulmonary Emboli

A

Usually arise from thrombophlebitis of veins in lower extremity

93
Q

Systemic (arterial) Emboli

A

Originate in the left circulation

  • Left heart: thrombi after MI, Endocarditis, or Dysrhythmias
  • Renal Emboli
  • Mesenteric Emboli
  • Coronary Emboli
  • Cerebral Emboli
94
Q

Thromboembolic Disease Treatment

A
  • Administration of anticoagulants to prevent clot formation: Aspirin, Heparin, Warfarin
  • Clot Busters
  • Slow or stop thrombus growth (aggressive reversal of risk factors)
95
Q

Varicose Veins

A

Distended, tortuous, and palpable

  • Caused by damage to one or more venous valves due to standing for extended periods of time and the contributing force of gravity
  • A damage valve permits back flow of blood (venous incompetence) and distended veins
  • Because vein becomes swollen, the surrounding tissues become edematous
  • Can progress to chronic venous insufficiency
96
Q

Venous Thrombi

A

With age, deep veins become susceptible to thrombi (Deep Vein Thrombosis)

  • DVT is often asymptomatic, but can lead to pulmonary emboli
  • Treatment: thrombolytics, anti-embolism stockings, avoid prolonged sitting/immobility
97
Q

Hypertension

A

Caused by increase in cardiac output, total peripheral resistance or both

  • Cardiac output: increase in heart rate or stroke volume
  • Peripheral resistance: increase in blood viscosity or reduction in vessel diameter, total length of vessels
  • Types: primary, secondary, and complicated
98
Q

Primary (“essential”) Hypertension

A

The cause is unknown (multifactorial)

  • 90-95% of patients
  • Contributing factors: family history, age, gender, race, diet, diabetes, obesity, cigarettes, heavy alcohol consumption
99
Q

Secondary Hypertension

Renal

A
  • Renal vascular stenosis
  • Renin-producing tumors
  • Renal failure
  • Primary sodium retention
100
Q 
Secondary Hypertension
(Endocrine)
A
  • Acromegaly

- Thyroid/Adrenal disorders

101
Q

Secondary Hypertension

Vascular

A
  • Arteriosclerosis

- Constriction of the aorta

102
Q

Secondary Hypertension

Pregnancy Induced/PIH

A
  • Pre-eclampsia

- Eclampsia

103
Q

Secondary Hypertension

Stress

A
  • Epinephrine
  • Norepinephrine
  • Glucocorticoids (cortisol)
104
Q

Complicated Hypertension

A

Demonstrates pathologic effects beyond hemodynamic alterations

  • Vascular remodeling (smooth muscle hypertrophy)
  • Hypoperfusion: heart, kidneys, eyes and brain
  • Examples: aneurysm rupture, arteriosclerosis, vessel occlusion, uremia, left ventricular enlargement
105
Q

Treatments for Hypertension

A

Eliminating risk factors
Pharmacologic:
- Diuretics: decrease blood volume and cardiac output
- ACE inhibitors and Angiotensin II RC Blockers: block the renin-angiotensin-aldosterone system
- Drugs which relax blood vessel smooth muscle: Ca++ channel blockers prevents smooth muscle contraction
Beta-blockers block catecholamines effects at beta-adrenergic RCS

106
Q

Orthostatic (Postural) Hypotension

A
  • Decrease in systolic and diastolic arterial blood pressure upon standing from a reclining position
  • The vasoconstrictive response to changing blood pressure and blood flow is inadequate, and dizziness results
  • Causes: age, drugs (antihypertensive and antidepressant therapy), volume depletion, prolonged immobility (chronic illness), starvation, physical exhaustion
107
Q

Aneurysms

A

A dilation or pouching of a vessel wall or cardiac chamber

  • As tension increases, the wall becomes thinner
  • True aneurysms involve all three layers
  • 2 types: Saccular/Berry, Fusiform
108
Q

Arteriosclerosis

A

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

  • Smooth muscle cells and collagen fibers migrate into the tunica interna, causing it to stiffen and thicken
  • This restricts the artery’s ability to change lumen size (increased vascular resistance)
109
Q

Atherosclerosis

A

A form of arteriosclerosis; inflammatory disease

  • Thickening and hardening of the vessel walls are caused by deposits of intra-arterial fat (LDL cholesterol) and fibrin that harden over time
  • Not a single disease; it varies depending on location, age, and genetics
110
Q

Atherosclerosis Stages

A

1- Endothelial injury
2- Fatty streak
3- Fibrous plaque
4- Complicated lesion

111
Q

Atherosclerosis

Stage 1

A

Endothelial Injury
- Smoking, high cholesterol, hypertension
Endothelial cells
- Decreased release of antithrombotic and vasodilating cytokines
- Increased release of inflammatory cytokines (TNF, interferon, and interleukins)
- Increased release of growth factors (smooth muscle proliferates)

112
Q

Progression of Atherosclerosis

A

Macrophages adhere to the injured endothelium

  • Release enzymes and toxic oxygen free radicals
  • Free radicals oxidize low density lipoprotein (LDL)
  • This oxidized LDL is toxic to endothelial cells
113
Q

Atherosclerosis

Stage 2

A

Fatty Streak: an accumulation of Foam Cells

  • Macrophages engulf oxidized LDL
  • The macrophages filled with oxidized LDL are called Foam Cells
  • These produce even more oxygen free radicals
114
Q

Atherosclerosis

Stage 3

A

The Fibrous Plaque

  • Under the influence of growth factors, smooth muscle cells proliferate
  • Smooth muscle migrates over the fatty streak, forming a cap (Fibrous Plaque)
115
Q

Atherosclerosis

Stage 4

A

Complicated Lesion

  • Fibrous Plaques aren’t stable: ulcerations, calcifications, apoptosis causes rupture
  • Platelets now have an adherence site and become activated
116
Q

Thromboangiitis Obliterans

Buerger Disease

A

An inflammatory autoimmune disease of the peripheral arteries of the hands and feet resulting in the formation of Non-Atherosclerotic lesions which obliterate the vessel

  • Causes pain and hair loss (not on the head) in young men who use tobacco
  • Progresses to ulcers and gangrenous lesions of fingers/toes
117
Q

Raynaud Disease

A

A primary vasospastic disorder of unknown etiology causing episodic vasospasm in arteries of the fingers, and less commonly the toes (pallor/cyanosis)

  • Vasospasms cause pallor, numbness, and cold sensations in the digits
  • Cyanosis can also appear
  • There is a cycle of pallor, cyanosis, the rubor due to vasospasm, followed by relaxation
  • Treatment is to remove the stimulus
118
Q

Raynaud Phenomenon

A

The same as Raynaud Disease, but it is secondary to other systemic diseases
- Collagen vascular disease (scleroderma), smoking, pulmonary hypertension, and environmental factors (cold, prolonged exposure to vibrating machinery)

119
Q

Coronary Artery Disease

CAD

A

Diminishes the myocardial blood supply
Can lead to:
- Reversible myocardial ischemia (angina)
- Irreversible myocardial infarction and death
- Both inhibit and pumping ability of the heart (either temporary or permanent) due to lack of O2 and nutrients

120
Q

Risk Factors for CAD

A 
Major
  - Increased age
  - Family history
  - Males or post menopausal females
Modifiable
  - Dyslipidemia
  - Hypertension
  - Cigarette smoking
  - Diabetes mellitus
  - Obesity/sedentary lifestyle
  - Atherogenic diet
121
Q

Myocardial Ischemia

A
  • Most commonly caused by atherosclerosis
  • Mass of plaque, platelets, fibrin and debris eventually narrows the artery lumen
  • Vasoconstriction encourages symptoms
122
Q

Silent Ischemia

A

An ischemia without pain

- Especially in diabetics

123
Q

Myocardial Infarction

A

Death of heart muscle

  • Myocardial cells become ischemic within 10 seconds of a blockage
  • Cells remain viable for 20 minutes
  • If the arteries can’t compensate for lack of O2, myocardial infarction is the result
124
Q

Complications of MI

A
  • Variable and depend on the location and extent of necrosis
  • Dysrhythmias
  • Pulmonary congestion
  • Reduced myocardial contractility
  • Inflammation of the pericardium
  • Pain
  • Fever
  • Pleural effusion
  • Pulmonary emboli and strokes
125
Q

Acute Pericarditis

A

When pericardial membranes become inflamed, and may produce an exudate

  • Usually a local manifestation of another disorder
  • Signs and symptoms: “Pleuritic” chest pain, pericardial “friction rub”
  • Treatment: analgesics and NSAIDs
126
Q

“Pleuritic” Chest Pain

A

Worsens with respiratory movements

127
Q

Pericardial Effusion

A

An accumulation of fluid in the pericardial cavity accompanying all types of pericarditis
- Signs and symptoms depend on severity and range from mild, pleuritic chest pain to compression of the heart causing reduced cardiac output, hypotension and even death

128
Q

Cardiac Tamponade

A

Occurs when the pressure from the pericardial fluid equals the diastolic filling pressure

  • In situations of severe trauma, a large pericardial effusion of fluid or blood cal lead to a serious compression of the heart
  • Right side of heart effected first
  • Treatment: emergency pericardiocentesis
129
Q

Constrictive Pericarditis

A
  • Fibrous scarring with possible calcification of the pericardium causes the visceral and pericardial layers to adhere to one another
  • Slower and more insidious onset and progression than Tamponade
  • Heart becomes constricted and reduces the cardiac output
  • Surgical removal of the pericardium may be required
130
Q

Cardiomyopathies

A

Diseases that affect the myocardium

  • Often the results of infarction, longstanding hypertension, infections, toxins, connective tissue diseases, proliferative disorders or nutritional deficiencies
  • Categories: Ischemic, Hypertrophic, Restrictive, and Dilated
131
Q

Hypertrophic Cardiomyopathy

A

Thickening of the myocardium, often a result of hypertension and valve disease

132
Q

Restrictive Cardiomyopathy

A
  • Due to infiltrative disease
  • The ventricular walls are excessively rigid and impede ventricular filling
  • No thickening of myocardium
  • Another common cause of heart failure in many under-developed countries
133
Q

Dilated Cardiomyopathy

A

Ischemic is the most common type

  • Remodeling due to overfilling and weak myocardial contractions
  • Enlarging of heart without thickening of myocardium
  • Often the end result of the other cardiomyopathies
134
Q

Valvular Stenosis

A

When any valve orifice is constricted or narrowed

  • The stenosis increases the workload of the chamber behind the valve and causes myocardial hypertrophy
  • Caused by calcification of degeneration of a valve
135
Q

Left-sided Valvular Disease

A

Most common

  • Aortic Stenosis
  • Mitral Stenosis
136
Q

Aortic Stenosis

AS

A
  • Low stroke volume
  • Left ventricular hypertrophy
  • Systolic murmur
137
Q

Mitral Stenosis

MS

A
  • Left atrial dilation
  • Pulmonary hypertension
  • Most commonly caused by acute rheumatic fever
  • 2-3x more common in women
  • Diastolic murmur
138
Q

Valvular Regurgitation

A

AKA valvular insufficiency or incompetence

  • When the cusps/leaflets of the valves fail to close, it permits backflow of blood during systole
  • Increased workload of pumping the blood “twice” causes myocardial HYPERTROPHY
  • All 4 valves can be affected, but the left valves are most common
139
Q

Aortic Regurgitation

AR

A
  • Widened pulse pressure
  • Dyspnea
  • Throbbing peripheral pulse
  • Diastolic murmur (backflow during diastole)
  • Dysrhythmias and endocarditis are common complications
140
Q

Mitral Regurgitation

MR

A
  • Pulmonary HTN
  • Systolic murmur (backflow during systole)
  • Left and right ventricle failure
141
Q

Tricuspid Regurgitation

A
  • Right heart failure
  • Edema
  • Systolic murmur (backflow during systole)
142
Q

Mitral Valve Prolapse

MVP

A

Autosomal dominant disorder where the anterior and posterior mitral cusps prolapse into the left atrium during left ventricular systole

  • Usually asymptomatic
  • Can cause endocarditis, chest pain, and dysrhythmias
  • In severe cases, signs and symptoms are similar to those of mitral regurgitation
143
Q

Rheumatic Heart Disease

RHD

A

Hypersensitivity reaction (type II) that occurs in 1-3% of cases of untreated strep infections

  • Manifests as a systemic inflammatory attack on the heart and many other tissues in the body
  • Carditis of all 3 layers of the heart wall
  • Inflammation of the endocardium
  • Vegetative growths on valves and granulomas in the myocardium
  • Signs and symptoms: fever, lymphadenopathy, chorea, truncal rash, high anti-streptolysin O titer, leukocytosis, elevated C-reactive protein, and ECG abnormalities
144
Q

Infective Endocarditis

A

Inflammation of the endocardium

  • Caused by Streptococci, Staphylococci, viruses, fungi, or Rickettsiae that enter the bloodstream
  • Risk factors: prior endothelial damage to valves, mitral valve, prolapse, prosthetic valves, septal defects, microbial colonization to damaged valve, adherence of microbes to form endocardial vegetations
  • IV drug abuse is the most common risk factor
145
Q

Rheumatic Heart Disease Manifestations

RHD

A
  • Fever
  • Lymphadenopathy
  • Chorea
  • Truncal rash
  • High anti-streptolysin O titer
  • Leukocytosis
  • Elevated C-reactive protein
  • ECG abnormalities
146
Q

Infective Endocarditis

Manifestations and Treatment

A
  • Fever
  • Cardiac murmur
  • Positive blood cultures
  • ECG abnormalities
  • Treatment: long-term anti-microbial therapy, prophylactic antibiotics for procedures that increase risk bacteremia
147
Q

Dysrhythmias

A

Classified by abnormalities of rate or rhythm

  • Can cause heart failure due to impairment of normal heart pumping
  • Hypotension, dizziness, chest pain, feeling of impending doom
148
Q

Tachycardia

A

> 100 bpm

149
Q

Bradycardia

A

< 50 bpm

150
Q

Atrial Fibrillation/Flutter

A
  • Decreased ventricular filling leads to 20% drop in cardiac output
  • Risk of blood clot embolisms
  • Treated by cardioversion or with “watchful waiting”
151
Q

Ventricular Tachycardia

VT

A
  • Refers to any rhythm faster than 100 bpm arising distal from the AV bundle
  • Usually hemodynamically unstable and required immediate treatment (usually cardiversion)
152
Q

Heart Failure

A

A dysfunction of cardiac muscle contractility that results in inadequate cardiac output and hypoperfusion of tissues

  • Failure of ventricle is failure of the pump
  • Left sided (most common): congestive heart failure
  • Right sided (less common): cor pulmonale
153
Q

Congestive (Left-Sided) Heart Failure

A

Failure of left ventricle leads to disorders of the lungs and pulmonary vessels
Manifestations:
- Fatigue
- Dyspnea
- Pulmonary edema, orthopnea, and a cough with frothy, blood-tinged discharge
- Cyanosis
- Rales (crackles)

154
Q

Cor Pulmonale

A 
Right-sided heart failure leads to systemic problems
Manifestations:
  - Fatigue
  - Ascites (accumulation of fluid in abdominal cavity)
  - GI disorders
  - Liver and spleen enlargement
  - Cyanosis
  - Distended jugular veins
  - Elevated venous pressure
  - Peripheral and systemic edema
155
Q

Shock

A

Anything that causes hypoperfusion of the vital organs, and will progress to death unless there is compensation for the abnormalities

  • General symptoms: “feeling sick”, weak, cold and hot simultaneously, nauseated, dizzy, confused, thirsty, and short of breath
  • Clinical signs: decreased blood pressure, decreased cardiac output, and decreased urinary output
156
Q

Cardiogenic Shock

A

The heart isn’t working

  • Ischemia
  • MI
  • Myocardial or Pericardial infections
  • Dysrhythmias
157
Q

Hypovolemic Shock

A

Insufficient intravascular fluid volume from loss of whole blood, blood plasma, interstitial fluid, or fluid sequestration outside the arterial vasculature

158
Q

Neurogenic/Vasogenic Shock

A

Widespread vasodilation from parasympathetic overstimulation and sympathetic understimulation

  • Causes: trauma to the spinal cord or medulla, depressive drugs, anesthetic agents, and severe emotional stress and pain
  • Persistant vasodilation causing RELATIVE HYPOVOLEMIA
159
Q

Anaphylactic Shock

A

Widespread Type I hypersensitivity reaction leading to vasodilation
- Also causes relative hypovolemia

160
Q

Septic Shock

A

Bacteremia

  • Endotoxins and Exotoxins cause the host to initiate a sever inflammatory process leading to widespread vasodilation and vascular collapse
  • Also causing relative hypovolemia
161
Q

Multiple Organ Dysfunction Syndrome

MODS

A

Progressive dysfunction of 2 or more organ systems resulting from an uncontrolled inflammatory response to sever illness or injury

  • Most common cause of mortality in intensive care units
  • Most common cause is sepsis and septic shock
  • Other triggers: severe trauma, burns, acute pancreatitis, obstetric complications, major surgery, circulatory shock, some drugs, and gangrenous or necrotic tissue
162
Q

Multiple Organ Dysfunction

Clinical manifestations

A

Often a predictable pattern

  • After inciting event, patient develops a low-grade fever, tachycardia, dyspnea, altered mental status, and hyperdynamic and hypermetabolic stress
  • Lung often 1st organ to fail resulting in tachypnea, pulmonary edema with crackles and hypoxemia
163
Q

Cause of MODS

A
  • Inflammatory responses are triggered damaging the vascular endothelium
  • Endothelium leaks fluid and protein into interstitial space resulting in hypotension and hypoperfusion
  • Damaged endothelium activates platelets and tissue thromboplastin leading to systemic microvasculature coagulation that may lead to DIC
  • Complement, coagulation, and kinin systems are activated leading to a hyperinflammatory and hypercoagulative state (interstitial edema, cardiovascular instability, endothelial damage, and clotting abnormalities)
  • Decreased O2 delivery
  • Hypermetabolism starts as a compensatory mechanism but leads to consumption of needed O2 to cells
164
Q

Multiple Organ Dysfunction

7-10 days

A

Beginning of Liver and Renal failure

  • Jaundice, abdominal distention, hepatic encephalopathy
  • Oliguria, uremia, and edema
165
Q

Multiple Organ Dysfunction

14-24 days

A

Liver and Renal failure progress

  • Gi system involvement with damage to the gut mucosa
  • Bacteria and toxins move into the portal and systemic systems
  • Hematologic and myocardial failure follow
  • Death may occur from 14 days to several weeks after inciting event
  • Mortality 30-100%
166
Q

Fetal Circulation

A
  • Developing fetus has special circulatory requirements because their lungs, kidneys and digestive tract are non-functional
  • Fetus derives its oxygen and nutrients and eliminates wastes through the maternal blood supply by way of the placenta
  • Normally there is no maternal/fetal mixing
  • The fetus is dependent on capillary exchange
167
Q

Fetal Circulation

sequence

A
  • Placenta
  • Umbilical vein
  • Ductus venosus between umbilical vein and inferior vena cava (bypasses the liver)
  • Inferior vena cava to heart (foramen ovale bypasses the lungs, ductus arteriosus bypasses the lungs)
  • Aorta
  • Umbilical arteries
168
Q

Congenital Heart Defects

A
  • Numerous causes
  • Most critical time is embryonic week 3 to week 8
  • Right to Left shunts result in hypoxia and cyanosis
  • Left to Right shunts result in overload of pulmonary hypertension and right heart failure
169
Q

Patent Ductus Arteriosus

A

Failure of the Dutus Arteriosus to close within the 1st few weeks of life

  • This increases the pressure in the pulmonary trunk and overworks the ventricles
  • Blood flows from the aorta (high pressure) to lower pressure pulmonary artery (left to right)
  • Patients present with a murmur and pulmonary vascular obstructive disease
170
Q

Atrial Septal Defect

ASD

A
  • Failure of interatrial septum to properly form
  • Left to right shunt
  • Cardiomegaly and pulmonary vascular congestion will be a result
171
Q

Patent Foramen Ovale

PFO

A

Foramen Ovale fails to close

  • Not a congenital heart defect, because foramen ovale is a normal structure
  • Usually asymptomatic
172
Q

Ventricular Septal Defect

VSD

A

Defect in the intraventricular septum

  • Most common type of congenital heart defect
  • In large VSDs, pressures become equal, blood flows into the right ventricle due to systemic pressures, and large amounts of blood flow into the pulmonary vessels
  • Contributes to enlargement of the left ventricle
173
Q

Tetralogy of Fallot

A

1- Pulmonary valve stenosis: blocks normal blood flow to lungs
2- Overriding aorta: emerges from both ventricles
3- Ventricular septal defect
4- Right ventricular hypertrophy

The patient is often kept alive only because of mixing of blood in what turns out to be a common ventricle

174
Q

Coarctation of the Aorta

A
  • Congenital malformation causing narrowing of the aorta
  • If the defect occurs near the ductus arteriosus, it will cause increased blood flow to the head and upper extremities and a decreased blood flow in the lower extremities
  • Left heart failure is a potential result
175
Q

Transposition of the Great Vessels

A

A switch between the pulmonary and the systemic circulation

  • Aorta emerges from the right ventricle
  • Pulmonary artery emerges from the left ventricle
  • 2 completely separate pump systems where the blood never mixes
  • Right side pumps blood from the body back to the body
  • Left side pumps blood from lungs back to lungs
  • Without septal defects to allow some mixing of blood, this would be incompatible with life

Pathophysiology (11 decks)

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