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Patho Summer 2024 > Exam 1 Edema, Electrolytes, A/B, Cardiac > Flashcards

Exam 1 Edema, Electrolytes, A/B, Cardiac Flashcards

1
Q

What barorecptors monitor BP?

A

Carotid sinus and aortic arch

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2
Q

What apparatus monitors pressure changes?

A

Juxtaglomerular

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3
Q

The baroreceptors of heart activate what mechanisms?

A

Neural, RAAS, ANP, ADH

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4
Q

How does the body regulate fluid volume and composition both intracelluarly and extracellularly?

A

By regulating volume and composition of blood

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5
Q

What is the dominant ECF cation?

A

Na+

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6
Q

What is responsible for 90-95% of osmotic pressure in ECF?

A

Na+

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7
Q

What does osmolality measure?

A

Concentration

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8
Q

What does osmolality regulation depend on?

A

How much water is present

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9
Q

What is the primary hormonal control of osmolality?

A

ADH

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10
Q

What forces favor filatration?

A

Capillary hydrostatic pressure (blood pressure)
Interstitial oncotic pressure (water-pulling)

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11
Q

What forces favor reabsorption?

A

Plasma oncotic pressure (water-pulling)
Interstitial hydrostatic pressure

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12
Q

ECF volume may vary even if osmolality of ECF is maintained? T or F

A

True

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13
Q

What is accumulation of fluid within the interstitial spaces?

A

Edema

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14
Q

What are causes of edema?

A

Increase in hydrostatic pressure
Losses or dim production of plasma albumin
Increases in capillary permeability
Lymph obstruction

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15
Q

What are the local clinical manifestations of edema?

A

Limited to site of trauma
Includes cerebral, pulmonary, pleural effusion, pericardial effusion, ascites

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16
Q

What are the generalized clinical manifestations of edema?

A

More systemic
Dependent edema accumulates in a gravity dependent manner

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17
Q

Other clinical manifestations of edema

A

Increased distance for diffusion of O2 so less gets to cells
Decreased blood flow leads to poor wound healing
Dehydration due to fluid not available for metabolis or perfusion

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18
Q

What is an example of edema?

A

Fluid sequestration following severe burns leads to shock

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19
Q

What is tightly regulated ECF due to influences on volume?

A

Na+

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20
Q

Small quantities of Na+ are lost in what?

A

Sweat= water, Na+, urea, Cl-, K+, NH3

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21
Q

What happens when Na+ is low and H2O moves into cells?

A

Hypotonic- cell swell

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22
Q

What happens when Na+ is too high and water moves out of cell?

A

Hypertonic solution- cell shrink

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23
Q

What happens with Na+ and water are stable in the cells?

A

Isotonic solution-no change

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24
Q

What are the 3 fluid compartments in the brain?

A

Blood
ECF and ICF
CSF

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25
Q

Is there a fixed volume in the cranium?

A

Yes

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26
Q

If you increase the fluid in one compartment in brain then what must happen to other two compartments?

A

Must decrease

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27
Q

Hyponatremia alters what function?

A

Neurlogic

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28
Q

Rapid shrinking can do what to the brain?

A

Tear vessels and cause hemorrhage

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29
Q

Rapid swelling can do what to the brain?

A

Herniation

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30
Q

What factors regulate Na+ retention?

A

Estrogens
Glucocorticoids
Osmotic diuretics
Poorly reabsorbed anions
Diuretic drugs
Dopamine

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31
Q

How does glucocorticoids regatulate Na+ retention?

A

Increase Na+ retention

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32
Q

How do osmotic diuretics regulate Na+ retention?

A

Decrease Na+ retention

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33
Q

How does poorly reabsorbed anions regulate Na+ retention?

A

Decrease Na+ retention

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34
Q

How does dopamine regulate Na+ retention?

A

Increases Na+ retention

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35
Q

Where is 98% of our total body K+ found?

A

Intracellular

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36
Q

What is circumferential range of K+?

A

0.3 range of 4.2 (3.9-4.5)

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37
Q

What is the major determinant of intracellular volume?

A

K+

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38
Q

What can serve as a outflow site for excess extracelluar fluid during hyperkalemia or hypokalemia?

A

Cells

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39
Q

What is 1st line of defense against changes in K+?

A

Redistribution

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40
Q

What does K+ establish with the heart?

A

Resting membrane potential

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41
Q

Low K+ will do what to the RMP?

A

Increase RMP (make it more negative)
Decrease excitability

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42
Q

High K+ will do what to the RMP?

A

Decrease RMP (makes it more pos)
Increase excitability

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43
Q

Acidosis will do what to the K+?

A

Increase it (hyperkalemia)

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44
Q

Alkalosis does what to the K+?

A

Lower K+ (hypokalemia)

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45
Q

K+ effects what ezymes?

A

Ones involved in carb metabolism and electron transport

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46
Q

How does increased aldosterone effect K+?

A

Causes K+ excretion
Increase permeability of luminal membrane permeability to K+

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47
Q

What disorders of aldosterone synthesis affect K+ regulation?

A

Addison’s Dx
Cohn’s Syndrome

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48
Q

How does K+ regulation effect tubular flow rate?

A

Increased tubular flow rate

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49
Q

The higher the concentration gradient then the more or less K+ is lost?

A

More

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50
Q

Hyperkalemia results from what?

A

Increased intake
Renal failure
Crushing injuries
Acidosis

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51
Q

What are symptoms of hyperkalemia?

A

muscular weakness
Irritability
Vent fib.
EKG changes

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52
Q

Hypolakemia results from what?

A

Excessive loss (diarrhea) or decreased intake
Kidney dx
Certain diuretics-lasix

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53
Q

Hypokalemia causes what symptoms?

A

Muscle fatigue
flaccid paralysis
mental confusion
Increased urine output
EKG changes

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54
Q

What is 99% of Ca+ found?

A

Bone

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55
Q

What stimulates osteocytes to deposit Ca+ within bone?

A

Calcitonin (CT)

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56
Q

What does Parathyroid hormone cause?

A

Bone resorption (osteoclasts)
Increase rental tubular reabsorption
Stimulates Vit D which increases intestinal absorption of Ca+

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57
Q

Acidosis frees Ca+ from what?

A

Proteins

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58
Q

Alkalosis will increase or decrease the percent of Ca+ bound to proteins?

A

Increase

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59
Q

How is most Ca+ excreted from body?

A

Feces (900-1000 mg/day)

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60
Q

Metabolic acidosis increases or decreases in Ca+ reabsorption?

A

Increases

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61
Q

Metabolic alkalosis increases or decreases Ca+ reabsorption?

A

Decreases

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62
Q

How does hypercalcemia affect the neuromuscular excitability and heart?

A

Causes neuromuscular excitability depression
Cardiac arrhythmias

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63
Q

Hypocalcemia has what affect on neuromuscular and heart?

A

Increase nerve and muscle excitability
Tetany

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64
Q

What changes the RMP?

A

K+

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65
Q

How does low K+ affect heart?

A

Decrease excitability
RMP more neg
Harder to get AP

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66
Q

How does high K+ affect RMP?

A

Increase excitability
Makes RMP more pos
Easily to excite and get AP

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67
Q

What does Ca+ effect in heart?

A

Threshold
By affecting Na+ entry into cells

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68
Q

How does high Ca+ affect threshold?

A

Increase threshold
Make cells less excitable
Harder to get AP

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69
Q

What are 3 ways the body regulates pH?

A

Chemical buffers (bicarbonate, proteins, phosphate)
Lungs
Kidneys

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70
Q

What is the main buffer in the ECF?

A

Bicarbonate

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71
Q

What is respiratory acidosis?

A

Low pH
High CO2

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72
Q

What is respiratory alkalosis?

A

High pH
Low CO2

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73
Q

What is metabolic acidosis?

A

Low pH
Low HCO3

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74
Q

What is metabolic alkalosis?

A

High pH
High HCO3

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75
Q

Normal anion gap?

A

8-16

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76
Q

What is normal anion gap?

A

Increased Cl-
Sum of Cl- and HCO3 normal
AKA hyperchloremic acidosis

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77
Q

Causes of normal anion gap ?

A

Diarrhea (most common)
Renal tubular dysfunction
Ammonia chorlide ingestion
Carbonic anhydrase inhibitors

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78
Q

What is increased anion gap?

A

Normal Cl-
Increased levels of unmeasured anions

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79
Q

What are examples of increased anion gap?

A

MUD PILERS
Methanol poisoning
Uremia (renal failure)
DKA (ketoacidiosis, starvation)
Pa-P-Aldehyde intoxication
Isoniazid
Lactic acidosis
Ethylene glycol poisoning (antifreeze)
Renal failure
Salicylate poisoning

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80
Q

Where is two thirds of the body’s water?

A

Intracellular fluid (ICF)

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81
Q

Where is one third of the body’s water?

A

Extracelluar fluid (ECF)

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82
Q

What are the two main components of the ECF?

A

Interstitial fluid and intravascular fluid (plasma/blood)

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83
Q

What is the standard value for total body water (TBW)?

A

60% of weight of 70 kg adult male

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84
Q

Hormonal regulation of Na+ balance is mediated by what?

A

Aldosterone

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85
Q

What happens in the kidneys when the blood pressure or blood volume is low?

A

Renin is released to convert AGI to AGII

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86
Q

What are the two main functions of AGII?

A

Vasoconstriction (increases BP)
Simulates secretion of aldosterone (promote Na+ and H20 reabsorption)

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87
Q

What is a major factor in regulating potassium?

A

Aldosterone

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88
Q

How does insulin affect K+?

A

Moves K+ into cells to lower K+ in blood by stimulating NaK pump

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89
Q

What provides the most efficient regulation of K+ balance over time?

A

Kidneys

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90
Q

What do principal cells in collecting duct do?

A

Secrete K+

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91
Q

What do intercalated cells in collecting duct do?

A

Reabsorbed K+

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92
Q

What hormone gets secreted due to low levels of Ca+?

A

Parathyroid hormone

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93
Q

What is anemia?

A

Decrease in # of circulating RBCs or decrease in quality or quantity of HGB

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94
Q

What is anemia a sign of?

A

Another underlying problem
It is not the primary issue

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95
Q

What are the causes of anemia?

A

Altered RBC production
Blood loss
Increased RBC destruction
Combination of all three

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96
Q

What is anemia classification based on?

A

Morphology

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97
Q

What is the size of RBC identified by?

A

Terms that end in “-cytic”
Macrocytic, Microcytic, normocytic

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98
Q

What is the hemoglobin content identified by?

A

Terms that end in “-chromic”
Normonchromic and hypochromic

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99
Q

What type of anemia is B12 or folate deficiency?

A

Macrocytic-Normochromic

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100
Q

What type of anemia is iron deficiency or thalassemia?

A

Microcytic-Hypochromic
Hgb don’t form properly

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101
Q

What type of anemia is hemorrhage, hemolytic, aplastic?

A

Normocytic-Normchromic

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102
Q

What is the genetic dx with low O2 and hgb forms irregular shape which clogs capillaries?

A

Sickle cell dx

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103
Q

What are the manifestations of anemia?

A

Hypoxia- fatigue, weakness, dyspnea, angina

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104
Q

How does the body compensation for anemia?

A

Attempts to increase cardiac output by increasing rate and strength of contraction

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105
Q

What is polycytemia?

A

Increase RBC production

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106
Q

What is difference between relative and absolute polycythemia?

A

Relative- blood thicker due to dehydration for example
Absolute- issue with erythropoietin so increases it

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107
Q

What is the issue with anemia in cardiac dx patients?

A

Increase HR to compensation can be bad for these pts

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108
Q

What is most compensation of anemia related to?

A

Cardiac

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109
Q

What happens in anemia?

A

Decrease O2 carrying capacity (hypoxemia)
Leads to tissue hypoxia

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110
Q

What is anemia of chronic dx?

A

Mild to moderate anemia from decreased erythropoiesis

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111
Q

What are some pathological mechanisms of anemia of chronic dx?

A

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

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112
Q

What is aplastic anemia?

A

Pancytopenia (reduction or absence of all 3 types of blood cells)
RBC, WBC, PLT

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113
Q

What type of disorders are most aplastic anemia?

A

Autoimmune disorders
Some are due to chemicals, drugs, physical agents

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114
Q

What is pathophysiology of aplastic anemia?

A

Hypocelluar bone marrow that has been replaced with fat

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115
Q

What are the signs of aplastic anemia?

A

Hypoexemia
Pallor (brownish pigment of skin)
Weakness
Fever
Dyspnea
Rapidly developing signs of hemorrhaging if plts affected

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116
Q

What is aplastic anemia a failure or suppression of?

A

Failure or suppression of bone marrow to produce adequate amounts of blood cells

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117
Q

What anemia is common due to drug effects?

A

Aplastic anemia

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118
Q

What drugs are known to cause aplastic anemia?

A

ABX (Chloramphenicol)
Anticonvulsants (Phenytoin, Mephenytoin)
Anti-inflammatories (ibuprofen)
Benzene

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119
Q

What is hemolytic anemia? What are 2 types?

A

Accelerated destruction of RBCs
Can be congenital (newborn) vs acquired (drug induced)

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120
Q

What is autoimmune hemolytic anemia?

A

Autoantibodies against antigens normally on surface of erythrocytes

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121
Q

What is a form of immune hemolytic anemia that is the result of allergic reaction to foreign antigens?

A

Drug induced hemolytic anemia
Called hapten model

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122
Q

What drugs can cause drug induced hemolytic anemia?

A

ABX
Penicillin
Cephalosporins (more than 90%)
Hydrocortisone

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123
Q

What is the drug induced hemolytic anemia called?

A

Hapten model

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124
Q

What is the hapten model with drug induced hemolytic anemia?

A

IgG antibody against drug or against unique antigen formed by interface of drug and erythrocyte protein is formed and binds to erythrocyte at normal body temperature

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125
Q

Where does hemolysis occur with drug induced hemolytic anemia?

A

Extravascular

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126
Q

What can rapidly resolve drug induced hemolytic anemia?

A

Cessation of drug administration

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127
Q

What are signs of drug induced hemolytic anemia?

A

Asymptomatic
Jaundice (icterus)
Aplastic crisis
Splenomegaly

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128
Q

What type of anemia is commonly noted in presence of CHF?

A

Anemia of chronic dx

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129
Q

How is hemolytic anemia divided into categories?

A

Congenital or acquired
Acquired is drug induced form

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130
Q

How does hemolytic anemia occur?

A

Occurs in blood vessls (intravascular) or lymphoid tissues (extravascular) that filter blood
Spleen or liver

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131
Q

What is intravascular hemolysis?

A

Least common
Caused by physical destruction of RBCs in circulation

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132
Q

What is extravascluar hemolysis?

A

Results from removal of damaged or opsonized RBCs by cells of mononuclear phagocyte system (MPS)

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133
Q

What is the most common type of megaloblastic anemia caused by vitamin B12 deficiency?

A

Pernicious anemia

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134
Q

What is folate deficiency anemia?

A

Impaired DNA synthesis secondary to folate deficiency cause megaloblastic cells with clumped nuclear chromatin
Folic acid is essential for RNA and DNA synthesis

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135
Q

What type of anemia is iron (fe) deficiency anemia?

A

Microcytic-Hypochromic anemia

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136
Q

What is the most common type of anemia worldwide?

A

Iron deficiency anemia

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137
Q

Who has higher risk for iron deficiency anemia? Males or females

A

Females

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138
Q

What are the 2 main causes of iron deficieny anemia?

A

Inadequate dietary intake
Excessive blood loss
(There is not intrinsic dysfunction of iron metabolism)
Both deplete iron stores & reduce iron metabolism

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139
Q

What is another cause of iron deficiency anemia?

A

Due to metabolic or function iron deficiency in which various metabolic disorders lead to either insufficient iron delivery to bone marrow or impaired iron use within marrow

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140
Q

What is the common cause of iron deficiency anemia in developed countries?

A

Pregnancy and chronic blood loss

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141
Q

Iron in the form on hgb is in constant demand by the body? T or F

A

True

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142
Q

How does blood loss affect iron?

A

Disrupts balance by creating need for iron which depletes iron stores more rapidly to replace iron lost from bleeding

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143
Q

How is iron deficiency related to supply and demand?

A

Occurs when demand for iron exceeds the supply of iron
Develops more slowly through 3 overlapping stages

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144
Q

What are the stages of iron deficiency anemia?

A

Stage 1: body’s iron stores are depleted (hgb content normal)
Stage 2: iron transport to bone marrow decreases
Stage 3: small hgb deficient cells enter circulation to replace normal age RBCs that are removed from circulation (s/sx occur)

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145
Q

What are signs of iron deficiency anemia?

A

Pallor skin and eyes
Brittle nails with spoon shape
Glossitis (tongue bald appearance with loss of papillae)

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146
Q

What converts fibrinogen to fibrin?

A

Thrombin

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147
Q

Where do we see most deficiency in clotting cascade?

A

Near the end of clotting cascade
Rarely see in beginning with TF

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148
Q

What is Vit C deficiency?

A

Lack of stable collagen

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149
Q

What patients have Vit C deficiency?

A

elderly
Alcoholics

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150
Q

What does hepatic failure cause?

A

Depletion of clotting factors

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151
Q

Where are almost all clotting factors made?

A

Liver

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152
Q

What is Vit K deficiency?

A

Depletion of factors 2 (prothrombin), 7, 9, 10, and protein C & S
II, VII, IX, X

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153
Q

What is Vit K deficiency due to?

A

Fat malabsorption due to lack of bile secretion

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154
Q

What is hemophilia A?

A

Deficiency of factor VIII (8)

155
Q

What is hemophilia B?

A

Deficiency of factor IX (9)

156
Q

What hemophilia is more common? A or B

157
Q

What is thrombocytopenia?

A

Low number of plts
Bleeding in small capillaries and blood vessels
Usually autoimmune disorder

158
Q

What is factor V Leiden mutation?

A

Mutation (R506Q) in heavy chain of factor V
Resistant to cleavage by activated protein C

159
Q

What does Factro V Leiden mutation result in?

A

Hypercoagulable state
Most common genetic risk factor for thrombosis in caucasians

160
Q

What are causes of thrombocytopenia? (Low plts)

A

Hypersplenism
Autoimmune dx
Hypothermia
Viral or bacterial infections that can cause DIC or HIT

161
Q

What are the two types of thrombocytopenia?

A

ITP (immune thrombocytopenia purpura)
TTP (thrombotic thrombocytopenia purpura)

162
Q

What is IgG antibody that targets platelets glycopteins and signs ?

A

immune thrombocytopenia purpura (ITP)
Petechia, purpura, progressing to major hemorrhage

163
Q

What is a thrombotic microangiopathy due to dysfunction of metalloproteinase ADAMTS13 enzyme?

A

Thrombotic thrombocytopenia purpura (TTP)

164
Q

What is essential (primary) thrombocythemia?

A

Too many plts
>600,000 plts
Myeloproliferative disorder of plt precursory cells
Megakaryocytes in bone marrow are produced in excess of

165
Q

What does platelet disorders result from?

A

Platelet membrane glycoprotein and von Willebrand factor deficiencies
Congenital or acquired

166
Q

What is Virchow’s Triad that contribute to thrombosis?

A

-Endothelia injury (causes HTN)
-Alterations/stasis in normal blood flow (causes atherosclerosis, valvular disorders, stasis)
-Hypercoagulability (increase plt function or increase clotting)

167
Q

What issues are associated with thrombosis?

A

Embolism
Infarction
DIC

168
Q

What is a complex acquired disorder in which clotting and hemorrhage occur simultaneously?

A

DIC (Disseminated Intravascular Coagulation)

169
Q

What happens with DIC?

A

Sudden onset of widespread thrombi in microcirculation with rapid consumption of plts and coagulation factors
Fibrinolysis is activated

170
Q

What is DIC unable to control?

A

Unable to control thrombi

171
Q

What is the primary initiator of DIC?

A

Endothelial damage

172
Q

What is the result of DIC with increase protease activity?

A

Result of increase protease activity in blood caused by unregulated generation of thrombin with subsequent fibrin formation and either accelerated or diminished fibrinolysis

173
Q

What does DIC result in?

A

Ischemia and hypoperfusion
Clot a lot then bleed a lot

174
Q

What increases in DIC?

A

Fibrin degradation product (FDP) and D-dimer levels which downregluates clotting
But causes bleeding

175
Q

What is mortality rate and treatment of DIC?

A

High mortality rate
TXT: try to remove stimulus

176
Q

What are signs of DIC?

A

Bleeding from venipuncture sites, arterial lines
Purpura, petechia, hematomas
Symmetric cyanosis of fingers and toes

177
Q

What are conditions associated with DIC?

A

Metastatic cancer
Acute bacterial and viral infections
Certain parasitic dx (malaria)
Sepsis/septic shock
Massive trauma
Burns
Products of conception

178
Q

How do the conditions associated with DIC begin it?

A

Damage to endothelium

179
Q

How does a patient get DIC?

A

-Due to initial endothelium damage leading to inflammatory cascade and massive activation of clotting cascade
-Widespread microvascular thrombisis which depletes factors
-Followed by bleeding due to depletion of factors and fibrinolysis

180
Q

How does patient transition from clotting to bleeding with DIC?

A

Stage 1: overactive clotting due to endothelium damage activating clotting cascade
Stage 2: run out of clotting factors and plts which leads to massive bleeding

181
Q

What determines the clinical course of DIC?

A

Intensity of stimulus, host response, comorbidities

182
Q

What is laboratory evidence of DIC?

A
  1. Clotting activation
  2. Fibrinolytic activation
  3. Coagulation inhibition consumption
  4. End organ damage/failure
183
Q

What is the most common condition associated with DIC?

184
Q

How does sepsis cause DIC?

A

Gram neg, gram pos organisms, or fungi damage vascular endothelium
Gram neg are primary cause of damage

185
Q

Does DIC cause local or widespread activation of coagulation cascade?

A

Widespread leading to clotting everywhere

186
Q

What is the common pathway for DIC?

A

Excessive and widespread exposure to TF (tissue factor)

187
Q

What are cause release of TF with DIC?

188
Q

How does bleeding locations occur with DIC?

A

Bleeding at 3 or more unrelated sites

189
Q

Which is more evident in DIC? Thrombosis or hemorrhage

A

Hemorrhage because it is more extensive and first observation
Sign of thrombosis are not always evident

190
Q

What is hemolytic dx of the newborn due to?

A

Occurs if antigens on fetal RBCs differ from antigens on mom RBCs

191
Q

What is patho of hemolytic dx of newborn?

A

Mom and fetus blood type different
Mom’s blood forms antibodies to fetal RBCs
Not problem with first pregnancy
Problem is with subsequent pregnancies

192
Q

What is the patho of sickle cell dx?

A

Deoxygenation of RBCs causing them to assume abnormal shape due to Hb S in cells

193
Q

What is chartacterized by intimal lesions called atheromas or fibrofatty plaques which protrude into and obstruct vascular lumens weakening underlying tunica media?

A

Atherosclerosis

194
Q

What contributes to more mortality (50%) in western world than any other disorder?

A

Atherosclerosis

195
Q

Who ends up with some plaque development?

196
Q

What are the 3 principle components of plaque?

A

Cells
ECM
Lipid

197
Q

What are the cells of plaque made up of?

A

Macrophages
Smooth muscle
Lymphocytes

198
Q

What is the primary cell in plaque?

A

Macrophages aka foam cells

199
Q

What is the ECM (extracellular matrix) of plaque made of?

200
Q

What indicates the stability of plaque?

A

Collagen
More stable then the more collagen

201
Q

What does the lipid component of plaque contain?

A

LDL
Oxidized LDL

202
Q

What is worst: LDL or oxidized LDL?

A

Oxidized LDL

203
Q

What happens with oxidized LDL?

A

Becomes free radical meaning extra e- present
Steals e- from others cells making them unstable

204
Q

Is a stable plaque good or bad?

A

Good
No acute events will occur

205
Q

What happens when stable plaque is disrupted?

A

Form blood clot acutely

206
Q

What is the layers of plaque?

A

Fibrous cap on top (lesions develop and cells die underneath)
Necrotic center underneath

207
Q

What are factors that induce or promote atherogenesis?

A

-Endothelial injury that alters normal homeostasis of endothelium
-Continuing inflammatory response
-Cyclic accumulation of cells and lipids

208
Q

What are possible causes of endothelial injury that include common risk factors for atherosclerosis?

A

Smoking
HTN
DM
Increased LDL (hyperlipidiemia)
Decreased HDL
Autoimmunity
Obesity

209
Q

What is the progression of atherosclerosis?

A
  1. Damaged endothelium
  2. Fatty streak
  3. Fibrous plaque
  4. Lesion
210
Q

What does damaged endothelium occur in atherosclerosis?

A

Injured endothelial cells become inflamed and cannot make normal amts of antithrombotic and vasodilating cytokines

211
Q

How does DM, smoking, and HTN cause atherosclerosis?

A

Contribute to increased LDL oxidation which causes toxic and cause smooth muscle proliferation

212
Q

What do macrophages do?

A

Engulf the LDL

213
Q

What happens when the foamy macrophages filled with LDL accumulate in significant amounts?

A

Fatty streak develops

214
Q

What happens when fatty streaks produce more oxygen radicals and cause damage to vessel wall?

A

Smooth muscle cells proliferate, produce collagen cap, and form fibrous plaque over fatty streak

215
Q

What are fibroblasts?

A

Cells that make collagen

216
Q

What happens with fibrous cap thins?

A

-Plaque/cap will rupture which initiates clotting cascade and forms a thrombus
-Thrombus may occlude vessel leading to ischemia and infarction

217
Q

What are the potential consequences of atheroclerosis?

A

-Narrow vessel leads to ischemia (Long term)
-Plaque hemorrhage or rupture caused by vessel obstruction (Acute)
-Thombosis lead to embolism (Acute)
-Aneurysmal dilation due to weak vessel wall

218
Q

How does atherosclerosis progress?

A

In a variety of ways

219
Q

What is the leading coronary artery & cerebrovascular dx?

A

Atherosclerosis

220
Q

What is atherosclerosis from?

A

Elevated plasma cholesterol/LDL levels

221
Q

What is the progression of plaque in atherosclerosis?

A

Lesions progress from endothelial injury to fatty streak to fibrotic plaque to complication lesion

222
Q

What is the main cause of atherosclerosis plaque devleopment?

A

Endothelial cell injury
Imbalance btw proinflammatory and anti-inflammatory mediators

223
Q

What is definition of HTN?

A

BP > 140/90

224
Q

What is primary HTN?

A

HTN is issue with no other underlying conditions
Complicated interaction btw genetics and environment

225
Q

What is the pathogenesis of HTN?

A

Increase CO
Increase peripheral resistance; increases afterload
Kidneys, RAAS, SNS all play a role

226
Q

What are consequences of HTN?

A

Vessel injury
Prolonged vasoconstriction
Target organ dx

227
Q

What is Liddle syndrome?

A

Genetic condition that leads to extreme HTN before puberty and into 20s
Defect in epithelial NA+ channel so not responsive to aldosterone

228
Q

What does HTN result from?

A

Na+ retention and elevated BP

229
Q

What does sustained HTN lead to?

A

Vascular remodeling (hylaine sclerosis and atherosclerosis)

230
Q

What does vascular remodeling lead to?

A

Retinal changes
Renal dx
Cardiac dx (CAD, CHF)
Neurological dx (stroke, dementia)

231
Q

What is SNS stimulation in HTN caused by?

A

Physiologic stress

232
Q

What is the role of the SNS in leading to HTN?

A

Causes:
increase HR and peripheral resistance
Increase insulin resistance (endothelial dysfunction)
Vascular remodeling (narrow vessels)
Procoagulant effects

233
Q

What factors lead to increased Na+ retention? (Decreased renal salt excretion so shift in pressure natriuresis relationship)

A

Genetics
Increase SNS
Increase RAAS
Endothelial dysfunction
Dysfunction of natriuretic hormones
Obesity
Renal glomerular and tubular inflammation
Insulin resistance
Increase Na intake
Decreased deitary K+, Mag, Ca+

234
Q

What is the pressure-natriuresis (PN) relationship and how is it shifted in HTN?

A

PN is abnormal because Na+ excretion is the same as in normotensive despite increased BP

235
Q

What hormones dysfunction with HTN?

A

Natriuretic hormones (ANP, BNP, CNP) which are unable to induce diuresis
Cause increase in vascular tone and shift PN relationship

236
Q

What happens when there is inadequate natriuretic function?

A

Serum levels of natriuretic peptides increase which are linked to increased risk for vent hypertrophy, atherosclerosis, HF

237
Q

What does salt retention lead to?

A

Salt retention leads to water retention and increases blood volume which causes increases in blood pressure

238
Q

How does obesity play a role in developing HTN?

A

Causes change in adipokines (leptin and adiponectin) and is associated with increased activity of SNS and RAAS

239
Q

What are the manifestations of HTN?

A

Atherosclerosis and LV hypertrophy

240
Q

What is LV hypertrophy a risk factor for?

A

Ischemic heart dx
Arrhythmias
CHF
Death

241
Q

What is one of the main long term consequence of HTN?

A

Ventricular remodeling

242
Q

What is ventricular remodeling and ultimately result in?

A

Involved both SNS and kidneys
Results in vasoconstriction, hypertrophy of LV, impaired contractility

243
Q

The early stages of HTN have no signs and is called what?

A

Lanthanic (silent) dx

244
Q

What are consequences of HTN?

245
Q

What are coronary heart dx aka CAD result from?

A

Myocardial ischemia

246
Q

When does CAD produce symptoms?

A

Until it is fairly advanced because of devleopment of collateral circulation along with plaque

247
Q

What is the leading cause of death among males and females?

248
Q

What is the patho of CAD?

A

Diminished coronary perfusion to myocardium relative to myocardium demand

249
Q

What are the risk factors for CAD?

A

Dyslipidemia
HTN
Smoking
DM and insulin resistance
Obese
Sedentary lifestyle
Atherogenic diet

250
Q

How does dyslipidemia influence plaque development and lead to CAD?

A

Abnormal concentration in lipoproteins
Increase LDL is strong indication of coronary risk
Low HDL is strong indication of coronary risk

251
Q

How does HTN influence plaque devleopment and cause CAD?

A

Causes endothelial injury and myocardial hypertrophy which increases myocardial demand
Causes overactivity of SNS and RAAS

252
Q

How does obesity influence plaque devleopment and lead to CAD?

A

Increased insulin resistance, decreased HDL, increased BP, inflammation
Change adipokines that affect cardiac risk

253
Q

What is metabolic syndrome?

A

A combination of obesity, dyslipidemia, HTN

254
Q

What does abominal obesity have a strong link to?

A

Increased CAD risk

255
Q

What are the categories of CAD?

A

Chronic Ischemic heart Disease (which is stable angina)
Acute coronary syndrome (which is unstable angina and myocardial infarction)

256
Q

What is plaque that is stable and chest pain that subsides with activity?

A

Stable angina aka angina pectoris

257
Q

What is plaque that is disrupted but stabilizes briefly?

A

Unstable angina

258
Q

What is plaque disruption that leads to thrombus formation?

A

Myocardial Infaraction

259
Q

What is the leading cause of death in U.S.

260
Q

What is patho of myocardial infaraction?

A
  1. Sudden change in plaque morphology
  2. Plt aggregation & activation and thrombus formation
  3. Occlusion of vessel within mins
  4. Hypoxic injury and if prolonged necrosis
261
Q

What is the biomarker measured with an heart disease?

262
Q

What is the biomarker level with unstable angina?

A

No increase in level

263
Q

What is the biomarker level with a Non-STEMI?

A

Increased biomarker level

264
Q

What is the biomarker level with STEMI?

A

Increased level

265
Q

What are consequences of MI?

A

Loss of blood supply to myocardium
Arrhythmias
CHF
Cardiogenic shock

266
Q

What does loss of critical blood supply to myocardium with an MI cause?

A

Hypoxia cell injury
Cell death/necrosis
Decreased function (don’t generate enough pressure)
Consequences of repair

267
Q

What do consequences of repair from an MI result in?

A

Fibrous scar tissue that lacks:
Contractility
Elastic
Conductive properties
(Can’t handle volume of generate enough pressure)

268
Q

What is sudden death in CHD patients often due to?

269
Q

How do arrhythmias occurs?

A

Ischemia induces heart muscle to become electrically unstable that it failts to contract in coordinated fashion or expel blood from heart

270
Q

What is arrhythmias most likely due to?

A

Dysregulation of ion balance across cardiomyocyte membrane

271
Q

What are the 3 types of cardiomypathies?

A

Dilated
Hypertrophic
Restrictive

272
Q

What is the issue with dilated cardiomyopathy (congestive cardiomyopathy)?

A

Volume issue
LV becomes dilated

273
Q

What are major symptoms of dilated cardiomyopathy?

A

Fatigue
Weakness
Palpitations

274
Q

What happens to contractility with dilated cardiomyopathy?

A

Decreased which impairs systolic function

275
Q

What are two types of hypertrophic cardiomyopathy?

A

Asymmetric sepal hypertrophy
Hypertensive (valvular hypertropic)

276
Q

What is asymmetric septal hypertrophy found in?

A

Kids who don’t know they have it until drop dead at sporting practice
Inherited heart defect

277
Q

What does asymmetric septal hypertrophy have?

A

Thicken septal wall that cause outflow obstruction of LVOT
Results in hyperdynamic state with exercise

278
Q

What does hypertensive (valvular hypertropic) cardiomyopathy occur from?

A

Increased resistance to vent ejection seen in HTN and valvular stenosis
Heart hypertrophy occurs to compensate

279
Q

What is restrictive cardiomyopathy from?

A

Inability of LV to expand
Muscle losses elsasticity and flexibility

280
Q

What is restricted with restrictive cardiomyopathy?

A

Filling of vent and reduced diastolic volume of either or both ventricles
Normal systolic function and wall thickness

281
Q

What are disorders of the endocardium?

A

Valve disorders
Rheumatic heart disease
Infective endocarditis

282
Q

Is infective endocarditis mainly bacterial or viral?

283
Q

What are the 3 hallmarks of infective endocarditis?

A

Endocardial damage
Bacterial adherence
Formation of vegetation

284
Q

What two factors in involved in patho of heart failure?

A

Decrease CO and subsuquent decrease in perfusion to other organs like kidneys
Compensatory mechanisms to maintain perfusion

285
Q

How does the compensatory mechanism helps a patient with HF?

A

They don’t. Makes HF worst

286
Q

What are the compensatory mechanisms of HF that we want to minimize?

A

Frank Starling
Increased SNS activity
RAAS
Myocardial hypertrophy

287
Q

Are any of the compensatory mechanisms for HF beneficial?

288
Q

What is the frank sterling mechanism and how does it affect HF?

A

Increase volume will increase stretch which will increase force of contraction
Makes HF worst

289
Q

Is the RAAS system long term or short term? Effect on HF?

A

Long term by retain Na+ to retain water
Makes HF worst

290
Q

What are the causes of heart failure?

A

Impaired cardiac function
Excess work demands

291
Q

What are examples of impaired cardiac function that cause HF?

A

MI
Valvular Dx

292
Q

What are examples of excess work demands that cause heart failure?

A

HTN
Anemia
Excess fluid administration

293
Q

What is valve stenosis?

A

Value is narrow and does not open all the way

294
Q

What is valve regurgitation?

A

Valve does not close all the way

295
Q

What value disorders affect systole?

A

AV stenosis
MV regurg

296
Q

What valve dirorders affect diastole?

A

MV stenosis
AV regurg

297
Q

What is congestive heart failure due to?

A

Failure of heart as a pump with accomplish congestion of body tissues

298
Q

Does congestive heart failure create a pos or neg feedback mechanism?

A

Pos feedback mechanism that progressively worsens

299
Q

What is the most common mechanical complication of an MI?

A

Left sided heart failure

300
Q

Mi leads to decreased contractility which does what to the preload and afterload?

A

Increase both

301
Q

What increases preload due to MI?

A

Decreased ejection fraction
Increased LVEDV

302
Q

What increases afterload due to MI?

A

Decreased renal perfusion
Increase renin and angiotensin

303
Q

What does R sided HF cause?

A

Congestion of peripheral tissue
Dependent edema and ascites and liver congestion

304
Q

What does L side HF cause?

A

Decreased CO- activity intolerance adn signs of decreased tissue perfusion
Pulmonary congestion-impaired gas exchange and orthopnea

305
Q

What leads to high output failure?

A

Anemia
Beriberi (Thiamine (B1) deficiency)
Sepsis
Hyperthyroidism (Graves dx)

306
Q

What does shock give rise to?

A

Systemic hypoperfusion caused by either reduction in CO or in the effective circulating blood volume

307
Q

What are the 4 types of shock?

A

Cardiogenic
Hypovolemic
Obstructive
Distributive

308
Q

What is hypovolemic shock?

A

Loss of blood volume, plasma, or ECF

309
Q

What happens to the pressure gradient with hypovolemic shock?

A

There is no more pressure gradient
It is lost so no blood flow

310
Q

When does hypovolemic shock begin?

A

When intravascular volume has decreased by about 15%

311
Q

What are the compensatory mechanisms for hypovolemic shock?

A

Fight or flight response
Redistribute blood from gut and skin to heart and brain
Catecholamine release (increase HR, SVR, contractility)
Shift of interstitial fluid
Adolsteorne, ADH released (retain Na+ so retains water)
Splenic discharge (disgorge stored RBCs

312
Q

What are the main hypoovemic shock compensatory mechanisms?

A

Increase HR
Vasoconstriction & increased SVR and afterload in order to imporove BP and perfuse vital organs

313
Q

What happens if compensatory mechanisms fail with hypovolemic shock?

A

Decreased tissue perfusion and cell death

314
Q

What are signs of hypovolemic shock?

A

High SVR
Rapid HR
Poor skin turgor
Increased thirst
Oliguria
Low systemic and pulmonary preload
Cool, clammy, pale skin

315
Q

What is Cardiogenic shock from?

A

Inability of heart to pump adequate blood to tissues and end organs

316
Q

What is the most common short term consequence of cardiogenic shock?

A

Acute MI
Severe episode of MI

317
Q

How is Cardiogenic shock defined?

A

Persistent HOTN and tissue hypoperfusion caused by cardiac dysfunction in presence of LV failure

318
Q

What are compensatory mechanisms for cardiogenic shock?

A

SNS Adrenergic (high HR, peripheral vasoconstriction, constrict splanchic to divert blood to heart and brain)
RAAS
Neurohormonal
Which all lead to fluid retention, systemic vasoconstriction, high HR

319
Q

What are hallmark signs of cardiogenic shock?

A

Tachy
Tachypnea
HOTN
JVD
Dysrthythmias
Low CO

320
Q

What happens with obstructive shock?

A

inability of heart to fill properly or obstruction to outflow from heart

321
Q

What are examples of obstructive shock?

A

Cardiac tamponade
Pericardial effusion
PE
Dissected aneurysm

322
Q

What is the issue with obstructive shock?

A

Restricts volume expansion/preload

323
Q

What is the issue with distributive shock?

A

Issues is blood vessels and not heart

324
Q

What does distributive shock cause loss of? And examples

A

Loss of sympathetic motor tone
Anaphylactic
Septic
Neurogenic

325
Q

How does distributive shock effect BP?

A

Decrease
Cause massive vasodilation

326
Q

How does anaphylactic shock occur?

A

Widespread hypersensitivity to allergen that triggers an allergic reaction

327
Q

What is released with anaphylactic shock and what does it cause?

A

Massive histamine release due to inflammatory response
Causes vasodilation
Presence of vasodilators

328
Q

What is septic shock due to?

A

Presence of inflammatory mediators
Bacterial infection

329
Q

What is the progressive of septic shock?

A

SIRS, sepsis, severe sepsis, then septic shock

330
Q

What is the compensatory mechanism for septic shock?

A

Anti-inflammatory response syndrome

331
Q

What are complications of shock?

A

ARDS (acute respiratory distress syndrome)
Acute renal failure
GI issues
DIC
MODS (multiple organ dysfunction syndrome)

332
Q

What happens to the tissue with septic shock?

A

Tissue hypoperfusion

333
Q

What is the initial problem with shock?

A

Decrease tissue perfusion

334
Q

What does decrease tissue perfusion in shock lead to?

A

Impaired oxygen and glucose delivery which impaired cellular metabolism

335
Q

What 2 things occur with impaired cellular metabolism due to shock?

A

Impaired oxygen delivery and use
Impaired glucose delivery and use

336
Q

What does impaired oxygen delivery and use lead to with shock?

A

Anaerobic metabolism which decreases ATP production and increases lactate

337
Q

What type of metabolism does shock become?

A

Shift to anaerobic metabolism

338
Q

What does impaired glucose delivery and use cause in shock?

A

Increase serum glucose and release of cathecholamiines, cortisol, GH

339
Q

What does shock cause overall?

A

Tissue ischemia (inadequate bf) and hypoxia (inadequate oxygen delivery) that leads to acidosis and cell dysfunction

340
Q

How is blood flow affected in hypovolemic and cardiogenic shock?

A

Bf distribution is reduced to skin, gut, and kidney to maintain blood flow to heart and brain

341
Q

How is blood flow effected with distributive shock?

A

Bf is unregulated through out skin and organ systems Vasodilation and increased cap permability are present

342
Q

How is cardiac output affected in obstructive shock?

A

Low CO caused by mechanical issue to bf such as tamponade, tension PTX, PE

343
Q

What is the leading cause of death in first year of life?

A

Congenital heart defect

344
Q

What are risk factors of congenital heart defects?

A

Prenatal, environment, genetics

345
Q

What are specific risk factors for congenital heart defects?

A

Material rubella
Insulin-dependent DM
Alcoholism
Phenylketonuria (PKU)
Hypercalcemia
Drugs
Chromosomal aberrations

346
Q

What are the classifications of congenital heart defects in kids?

A

Lesions increasing pulmonary bf
Lesions decreasing pulmonary bf
Obstructive lesions
Mixing lesions

347
Q

In congenital heart defects, how do lesions increase pulmonary blood flow and example of it?

A

Defects that shunt from high pressure left side to low pressure right side with pulmonary congestion; acysnois
Ex: Patent ductus arteriosus

348
Q

What happens in patent ductus arteriosus?

A

Shunt blood from high pressure left side to low pressure right side causing pulmonary congestion

349
Q

What are the 3 parts of circulation open in fetus?

A

Ductus venosus
Foramen ovale
Ductus arteriosus

350
Q

What does the 3 holes become when they close when baby takes first breath at birth?

A

Ductus venosus become ligamentum venosum
Foramen ovale becomes fossa ovalis
Ductus arteriosus becomes ligamentum arteriosus

351
Q

Where is the foramen ovale?

A

Opening that allows blood to bypass lungs and cross over from RA to LA since fetus lungs are non-functional full of fluid

352
Q

Where is the ductus arteriosus?

A

Connection between aorta and pulmonary trunk that allows oxygenated blood to bypass fetus nonfunctional lungs since mother supplies oxygenation blood thru placenta for fetus

353
Q

What congenital defects in kids increase pulmonary blood flow?

A

Patent ductus arteriosus (PDA)
Atria septal defect
Ventricular septal defect
Atrioventricular canal defect

354
Q

What does patent ductus arteriosus lead to?

A

Increased pulmonary venous return to LA and LV
Increased workload on left side of heart

355
Q

What congenital heart defects in kids decrease pulmonary blood flow?

A

Tetralogy of fallot (TOF)
Tricuspid Atresia

356
Q

What are the 4 specific defects seen with tetralogy of fallot in kids?

A
  1. Ventricle septal defect high in septum
  2. Overriding aorta that straddles VSD
  3. Pulmonary valve stenosis
  4. RV hypertrophy
357
Q

What is the most common cyanotic congenital heart defect in kids?

A

Tetralogy of fallot

358
Q

What does tricuspid atresia cause in kids?

A

Tricuspid valve that has no opening resulting in no way to get blood from RA to RV

359
Q

What do lesions that decrease pulmonary blood flow cause?

A

A complex right to left shunt and cyanosis

360
Q

What do obstructive lesions cause for congenital heart defects in kids?

A

Right or left sided outflow tract obstructions that curtail or prohibit blood flow out of heart
No shunting

361
Q

Is there shunting with obstructive lesions that cause congenital heart defects?

362
Q

What are examples of congenital heart defects that cause obstructive lesions?

A

Contraction of aorta
Hypoplastic left heart syndrome
Aortic/Pulmonary Stenosis

363
Q

What is coarctation of aorta?

A

Narrowing of lumen of aorta that impedes blood flow

364
Q

What is hypoplastic left heart syndrome?

A

Underdevelopment of left side heart stuctures

365
Q

What heart structures are underdevelopment in hypoplastic left heart syndrome?

A

LV
Aorta
Aortic arch
Mitral stenosis

366
Q

What do mixing lesions cause in congenital heart defects in kids?

A

Desaturated blood and saturated blood mix in chambers or great arteries of heart

367
Q

What are 2 examples of mixing lesions with congenital heart defects in kids?

A

Transposition of great arteries
Truncus arteriosus
Total Anomalous Pulmonary Venous Connection

368
Q

What is the condition where the aorta arises from the RV and the PA arises from the LV?

A

Transposition of great arteries

369
Q

What occurs with blood in transposition of great arteries?

A

Unoxygenated blood circulates continuously thru systemic circulation
Oxygenated blood circulates repeatedly thru pulmonary circulation

370
Q

What is transposition of great arteries incompatible with?

A

With life unless the 2 pathways have way to communicate

371
Q

What is it called when there is only one main artery arising from both ventricles?

A

Truncus arteriosus
Failure of large embryonic artery to divide into PA and aorta

372
Q

What are 2 common consequences of congenital heart defects in kids?

A

Heart failure
Hypoxemia

373
Q

Heart defects that allow desaturated blood to enter systemic systemic without passing thru lungs result in what 2 things?

A

Hypoxemia
Cyanosis

374
Q

What is it when the arterial oxygen tension is below normal and results in low oxygen artieral saturations?

375
Q

What is blue discoloration of mucous membranes and nail ends?

376
Q

What is cyanosis the result of in kids?

A

Deoxygenated hemoglobin

377
Q

What are signs of heart failure in kids?

A

Poor feeding and sucking
Failure to thrive
Dyspnea, tachypnea, diaphoresis, retractions, grunting, nasal flaring wheezing, coughing
Pallor or mottling
Hepatomegaly
Pulmonary overcirculation

378
Q

What is the predominate cause associated with congenital defects in kids?

A

Pulmonary overcirculation (pressure higher in lungs)

379
Q

What is pulmonary vascular resistance increases that exceed or equal vascular resistance which results in reversal of shunting?

A

Eisenmenger syndrome

380
Q

What are specific defects in kids that cause hypoxemia and cyanosis?

A

Lesions that obstruct and shunt from right to left side of heart
Defects involved in mixing saturated and unsaturated blood
Transposition of great arteries

381
Q

What type of hypoxemia is cyanosis only occasionally when stressed in kids?

A

Mild hypoxemia

382
Q

What type of hypoxemia is feeding intolerance, poor weight gain, tachypnea, and dyspnea seen in kids?

A

Severe hypoxemia

383
Q

What type of hypoxemia may kids be small for their age and have cognitive/motor skill delays?

A

Chronic hypoxemia

384
Q

What type of hypoxemia in kids will have polycythemia, SOB with exertion, easily fatigued, exercise intolerance, and clubbing of nail ends?

A

Chronic hypoxemia

Patho Summer 2024 (1 decks)

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