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
FSH
Ova/Sperm development and production
26
LH
Causes maturation of uterine lining, testosterone production, and ovulation
27
PRH
Stimulates release of Prolactin (PRL) from the Anterior Pituitary
28
PRL
Causes Lactation of mammary glands
29
Hypopituitarism
Caused by infarction of the gland, removal/destruction of pituitary, space occupying adenomas, aneurysms that cause compression - Effects depend on the affected hormone
30
Panhypopituitarism
Absence of all hormones from the Anterior Pituitary | - Treatment may consist of replacing HGH, ACTH, TSH, and sex hormones
31
Pituitary Dwarfism
Results from insufficient HGH release during an individual's growth phase - Patient has normal face and intelligence, with normal body proportions
32
Giantism
Caused by a Pituitary Adenoma - Excess HGH is released during an individual's growth phase - Now fairly rare because of early detection of Adenomas
33
Acromegaly
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)
34
Thyroid Gland
``` Secretes Thyroxine (T4) and Triiodothyronine (T3) - Stores a 100 day supply of hormones in sacs that make up most of the gland ```
35
Thyroid Hormones
- 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
36
Hypothyroidism
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
37
Hyperthyroidism
- 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
38
Goiter
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
39
Graves Disease
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
40
Thyrotoxic Crisis | "Thyroid Storm"
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)
41
Hashimoto Disease
Autoimmune destruction of the Thyroid Gland | - Primary Hypothyroid abnormality
42
Secondary causes of Hypothyroidism
- Toxic Thyroiditis from a bacterial infection of the Thyroid - Complication of Thyroid surgery
43
Myxedema
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
44
Myxedema Coma
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
45
Congenital Hypothyroidism | Cretinism
- 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
46
Parathyroid Glands
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
47
Hyperparathyroidism
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
48
Hypoparathyroidism
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
49
Diabetes Mellitus
- 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
50
Diabetes Mellitus | Type I
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
51
Diabetes Mellitus | Type II
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)
52
Glycosylated Hemoglobin | HbA1c
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%
53
Hypoglycemia and Insulin Shock
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
54
``` Diabetic Ketoacidosis (DKA) ```
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
55
Hyperosmolar Hyperglycemic Non-Ketotic Syndrome | HHNKS
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
56
Acute Complications of DM
- Hypoglycemia - Insulin Shock - DKA - HHNKS
57
Chronic Complications of DM
- Microvascular Disease - Macrovascular Disease - Peripheral Neuropathy - Infections - Retinopathy (blindness; leading cause) - Nephropathy (leading cause)
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Microvascular Disease in DM
A thickening of the capillary basement membrane; leading to decreased perfusion of tissues
59
Macrovascular Disease in DM
Manifests as a 2-4 fold increase in heart disease
60
Peripheral Neuropathy in DM
Results from multiple metabolic, genetic, and environmental factors, with over 60-70% of patients showing some form of nerve damage
61
Hormones of the Adrenal Cortex
- Glucocorticoids - Mineralocorticoids - Gonadocorticoids
62
Glucocorticoids
- 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
63
Cushing Disease/Syndrome
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
64
Mineralocorticoids
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+
65
Conn Disease
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)
66
Adrenogenital Syndrome in Women
Hypersecretion of weak androgens (DHEA) | - In women DHEA is masculinizing, causing deep voice and increased body hair
67
Gonadocorticoid Disorders
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
68
Virilization in Women
The clitoris is enlarged, and may resemble the male penis to the point that the sex of the child is questioned or mistake
69
Virilization in Men
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
70
Androgenital Syndrome in Men
Hypersecretion of estrogens | - In men Estrogens are feminizing, causing development of female secondary sex characteristics
71
Addison Disease
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
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Adrenal Medulla
- 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
Pheochromocytoma
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
Stress
- 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
Distress
Demand exceeds a person's coping abilities
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Stress is and Interaction Between...
Individual differences - Genes, development, experience Behavioral responses - Fight or flight, personal behavior: diet, smoking, drinking, exercise Physiologic response
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General Adaptation Syndrome Stages
- Alarm stage - Resistance (adaptation) stage - Exhaustion stage
78
Alarm Stage
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
The Resistance Stage
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
Cortisol | in the Resistance Stage
- 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
TSH | in the Resistance Stage
Increased Thyroxin (increased Basal Metabolic Rate)
82
Aldosterone | in the Resistance Stage
- Increases NA+ and water retention | - Increases blood volume and pressure
83
ADH
- Water retention | - Increases blood volume and pressure
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Exhaustion Stage
``` 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
Thrombus
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
Thrombophlebitis
Thrombi form in veins, with associated inflammation
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Thrombi of Heart Valves
Due to endocardial inflammation or rheumatic fever
88
Embolism
Obstruction of a vessel by moving chunk of material
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Thromboemboli
Thrombi which break loose and travel to another site
90
Air Emboli
Air bubble from injection, punctured lung, or open vessel
91
Fat Emboli
- Hip replacement surgery | - Broken bone
92
Pulmonary Emboli
Usually arise from thrombophlebitis of veins in lower extremity
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Systemic (arterial) Emboli
Originate in the left circulation - Left heart: thrombi after MI, Endocarditis, or Dysrhythmias - Renal Emboli - Mesenteric Emboli - Coronary Emboli - Cerebral Emboli
94
Thromboembolic Disease Treatment
- Administration of anticoagulants to prevent clot formation: Aspirin, Heparin, Warfarin - Clot Busters - Slow or stop thrombus growth (aggressive reversal of risk factors)
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Varicose Veins
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
Venous Thrombi
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
Hypertension
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
Primary ("essential") Hypertension
The cause is unknown (multifactorial) - 90-95% of patients - Contributing factors: family history, age, gender, race, diet, diabetes, obesity, cigarettes, heavy alcohol consumption
99
Secondary Hypertension | Renal
- Renal vascular stenosis - Renin-producing tumors - Renal failure - Primary sodium retention
100
``` Secondary Hypertension (Endocrine) ```
- Acromegaly | - Thyroid/Adrenal disorders
101
Secondary Hypertension | Vascular
- Arteriosclerosis | - Constriction of the aorta
102
Secondary Hypertension | Pregnancy Induced/PIH
- Pre-eclampsia | - Eclampsia
103
Secondary Hypertension | Stress
- Epinephrine - Norepinephrine - Glucocorticoids (cortisol)
104
Complicated Hypertension
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
Treatments for Hypertension
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
Orthostatic (Postural) Hypotension
- 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
Aneurysms
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
Arteriosclerosis
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
Atherosclerosis
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
Atherosclerosis Stages
1- Endothelial injury 2- Fatty streak 3- Fibrous plaque 4- Complicated lesion
111
Atherosclerosis | Stage 1
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
Progression of Atherosclerosis
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
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Atherosclerosis | Stage 2
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
Atherosclerosis | Stage 3
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
Atherosclerosis | Stage 4
Complicated Lesion - Fibrous Plaques aren't stable: ulcerations, calcifications, apoptosis causes rupture - Platelets now have an adherence site and become activated
116
Thromboangiitis Obliterans | Buerger Disease
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
Raynaud Disease
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
Raynaud Phenomenon
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
Coronary Artery Disease | CAD
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
Risk Factors for CAD
``` Major - Increased age - Family history - Males or post menopausal females Modifiable - Dyslipidemia - Hypertension - Cigarette smoking - Diabetes mellitus - Obesity/sedentary lifestyle - Atherogenic diet ```
121
Myocardial Ischemia
- Most commonly caused by atherosclerosis - Mass of plaque, platelets, fibrin and debris eventually narrows the artery lumen - Vasoconstriction encourages symptoms
122
Silent Ischemia
An ischemia without pain | - Especially in diabetics
123
Myocardial Infarction
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
Complications of MI
- 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
Acute Pericarditis
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
"Pleuritic" Chest Pain
Worsens with respiratory movements
127
Pericardial Effusion
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
Cardiac Tamponade
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
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Constrictive Pericarditis
- 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
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Cardiomyopathies
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
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Hypertrophic Cardiomyopathy
Thickening of the myocardium, often a result of hypertension and valve disease
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Restrictive Cardiomyopathy
- 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
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Dilated Cardiomyopathy
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
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Valvular Stenosis
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
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Left-sided Valvular Disease
Most common - Aortic Stenosis - Mitral Stenosis
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Aortic Stenosis | AS
- Low stroke volume - Left ventricular hypertrophy - Systolic murmur
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Mitral Stenosis | MS
- Left atrial dilation - Pulmonary hypertension - Most commonly caused by acute rheumatic fever - 2-3x more common in women - Diastolic murmur
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Valvular Regurgitation
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
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Aortic Regurgitation | AR
- Widened pulse pressure - Dyspnea - Throbbing peripheral pulse - Diastolic murmur (backflow during diastole) - Dysrhythmias and endocarditis are common complications
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Mitral Regurgitation | MR
- Pulmonary HTN - Systolic murmur (backflow during systole) - Left and right ventricle failure
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Tricuspid Regurgitation
- Right heart failure - Edema - Systolic murmur (backflow during systole)
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Mitral Valve Prolapse | MVP
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
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Rheumatic Heart Disease | RHD
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
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Infective Endocarditis
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
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Rheumatic Heart Disease Manifestations | RHD
- Fever - Lymphadenopathy - Chorea - Truncal rash - High anti-streptolysin O titer - Leukocytosis - Elevated C-reactive protein - ECG abnormalities
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Infective Endocarditis | Manifestations and Treatment
- Fever - Cardiac murmur - Positive blood cultures - ECG abnormalities - Treatment: long-term anti-microbial therapy, prophylactic antibiotics for procedures that increase risk bacteremia
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Dysrhythmias
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
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Tachycardia
> 100 bpm
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Bradycardia
< 50 bpm
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Atrial Fibrillation/Flutter
- Decreased ventricular filling leads to 20% drop in cardiac output - Risk of blood clot embolisms - Treated by cardioversion or with "watchful waiting"
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Ventricular Tachycardia | VT
- Refers to any rhythm faster than 100 bpm arising distal from the AV bundle - Usually hemodynamically unstable and required immediate treatment (usually cardiversion)
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Heart Failure
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
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Congestive (Left-Sided) Heart Failure
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)
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Cor Pulmonale
``` 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 ```
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Shock
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
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Cardiogenic Shock
The heart isn't working - Ischemia - MI - Myocardial or Pericardial infections - Dysrhythmias
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Hypovolemic Shock
Insufficient intravascular fluid volume from loss of whole blood, blood plasma, interstitial fluid, or fluid sequestration outside the arterial vasculature
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Neurogenic/Vasogenic Shock
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
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Anaphylactic Shock
Widespread Type I hypersensitivity reaction leading to vasodilation - Also causes relative hypovolemia
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Septic Shock
Bacteremia - Endotoxins and Exotoxins cause the host to initiate a sever inflammatory process leading to widespread vasodilation and vascular collapse - Also causing relative hypovolemia
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Multiple Organ Dysfunction Syndrome | MODS
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
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Multiple Organ Dysfunction | Clinical manifestations
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
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Cause of MODS
- 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
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Multiple Organ Dysfunction | 7-10 days
Beginning of Liver and Renal failure - Jaundice, abdominal distention, hepatic encephalopathy - Oliguria, uremia, and edema
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Multiple Organ Dysfunction | 14-24 days
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%
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Fetal Circulation
- 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
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Fetal Circulation | sequence
- 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
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Congenital Heart Defects
- 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
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Patent Ductus Arteriosus
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
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Atrial Septal Defect | ASD
- Failure of interatrial septum to properly form - Left to right shunt - Cardiomegaly and pulmonary vascular congestion will be a result
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Patent Foramen Ovale | PFO
Foramen Ovale fails to close - Not a congenital heart defect, because foramen ovale is a normal structure - Usually asymptomatic
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Ventricular Septal Defect | VSD
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
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Tetralogy of Fallot
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
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Coarctation of the Aorta
- 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
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Transposition of the Great Vessels
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