HESI Prep Flashcards
(276 cards)
1
Q
Risk Factors associated with Osteoporosis-lifestyle
A
sedentary calcium nutritional deficiency high protein diet excessive alcohol intake excessive caffeine intake smoking
2
Q
Risk Factors associated with Osteoporosis-drug and disease related
A
antacids (promote calcium excretion)
Anticonvulsants (promote calcium excretion)
Heparin
corticosteroids or cushing disease (promote calcium excretion)
Gastrectomy
COPD
Malignancy
Hyperthyroidism (accelerate bone turnover)
hyperparathyroidism
Rheumatoid Arthritis
3
Q
Explain the RANK receptor pathway
A
(Osteoblasts (formation) produce) RANKL+RANK=osteoclast (resorption) differentiation and proliferation
OPG is a competitor for RANKL receptor site, binds to RANK to block this pathway to keep bone resorption in check with bone formation.
4
Q
Diverticulosis
A
the mucosal layer of the colon herniates through the muscularis layer. most often occurs in the sigmoid colon.
5
Q
Diverticulitis
A
infected diverticula and abscesses
6
Q
Symptoms of Diverticulosis
A
lower left quadrant pain, nausea, vomitng, slight fever, elevated WBC
7
Q
What irritates diverticulosis?
A
the lower the volume in the colon, the more vigorous the contractions and thus more pressure on the haustra
8
Q
age over 40 constipation low dietary fiber connective tissue disorders (marfan syndrome, ehlers danlos) hereditary or genetic predisposition
A
Risk factors for diverticulosis
9
Q
Hyperosmolar Hyperglycemic State
aka hyperosmolar Hyperglycemic Nonketotic Syndrome
A
hyperglycemia blood glucose >600 mg/dL hyperosmolarity blood plasma >320 mOsm/L Dehydration absence of ketoacidosis depression of sensorium
10
Q
kidneys and glucose
A
normally, the kidneys try to make up for high glucose levels in the body by allowing the extra glucose to leave the body in the urine. If you do not drink enough fluids, or fluids that contain sugar, the kidneys can no longer get rid of the extra glucose. Glucose levels in the blood can become very high as a result. The blood then becomes much more concentrated than normal, resulting in hyperosmolarity.
11
Q
Hyperosmolarity
A
a conditoin in which blood has a high concentration of salt, glucose, and other substances that normally cause water to move INTO the bloodstream. This DRAWS WATER OUT OF ORGANS (including the brain). Hyperosmolarity creates a cycle of increasing blood glucose levels and dehydration.
12
Q
Risk factors for HHS
A
type 2 diabetes (insulin resistant kind)
acute pancreatitis
severe infection
myocardial infarction
13
Q
massive glucosuria brings about what?
A
water loss as water follows the glucose into the urine
14
Q
Manifestations of HHS
A
weakness dehydration polyuria excessive thirst neurological signs- hemiparesis, babinski reflexes, aphasia, muscle fasciculations, hyperthermia, hemianopia (loss of 1/2 visual field), nystagmus, hallucinations, seizures, coma
15
Q
The onset of HHS is often mistaken for what?
A
a stroke
16
Q
type 2 diabetes
A
most commom
fat, liver, and muscle cells do not respond correctly to insulin=insulin resistance
glucose does not gain access to those cells to provide energy
being overweight makes it harder for your body to utilize glucose properly
17
Q
Manifestations of diabetes
A
bladder, kidney, skin infections slow to heal fatigue hunger thirst polyuria blurred vision erectile dysfunction pain or numbness in hands and feet
18
Q
fasting blood glucose +
A
> 126 mg/dL twice
19
Q
hemoglobin A1C test +
A
> 6.5%
20
Q
oral glucose tolerance +
A
> 200 mg/dL two hours after drinking the special drink
21
Q
Type 1 diabetes
A
body fails to produce insulin
loss of pancreatic beta cells through autoimmune destruction
22
Q
osteoporosis
A
metabolic bone disease characterized by a loss of mineralized bone mass causing increased porosity of the skeleton and susceptibility to fractures
bone resorption outpaces bone formation
decreased intestinal absorption of calcium due to deficient vit D activation
23
Q
Estrogen deficiency
A
often leads to osteoporosis
decreased estrogen increases cytokines and decreases OPG
OPG inhibits the RANK receptor pathway which promotes osteoclast differentiation and proliferation
24
Q
hCG
Human chorionic gonadotropin
A
in the event of fertilization, hCG is produced by the trophoblastic cells in the blastocyst.
hCG prevents luteal regression.
25
Corpus luteum
remains functional for three months after fertilization
| provides hormonal support for pregnancy until the placenta is fully functional
26
Anterior pituitary releases FSH and LH
stimulate development of follicles
27
Starling's Laww
The maximum force of contraction and cardiac output is achieved when venous return produces an increased in left ventricular end-diastolic filling (preload) such that the muscle fibers are stretched about two and one-half times their normal resting length. When muscle fibers are stretched to this degree, there is optimal overlap of the actin and myosin filaments needed for maximal contraction.
28
length tension/frank starling mechanism
with increased diastolic filling, there is increased stretching of the myocardial fibers and more optimal approximation of the heads on the thick myosin filaments to the troponin binding sites on the thin actin filaments, this results in increased force for the next contraction
29
Starling and the Curce
increased contractility=increased CO curve moves up and to the left
decreased inotropy-curve moves down and to the right
30
heart failure
decreased in CO and renal blood flow leads to increased sodium and water retention, a resultant increase in vascular volume, and venous return to the heart, and an increase in ventricular end-diastolic volume (preload). The heart cant eject all this blood, and the back up accumulates in the lungs and atria.
31
Name the compensatory mechanisms in heart failure that function together to maintain CO for the failing heart.
frank starling mechanisms
sympathetic reflexes
RAAS
myocardial hypertrophy
32
why do we give diuretics to people with heart failure?
The use of diuretics in persons with heart failure helps to reduce vascular volume and ventricular filling, thereby unloading the heart and reducing ventricular wall tension.
33
How does the Frank Starling mechanism hurt heart function?
the increased muscle stretch increases ventricular wall tension and that makes the myocardial muscles consume more oxygen and can then produce ischemia and contribute to further impair inotropy. (curve moves back and to the right)
34
sympathetic Nervous System role in compensatory response to decreased CO
sympathetic nervous system helps maintain perfusion of the organs by direct stimulation of heart rate and cardiac contractility using EPI and NE, regulating vascular tone, and enhancement of renal sodium and water retention.
sympathetic response is meant to augment blood pressure and CO
35
When Sympathetic Nervous System compensation goes bad
an increase in sympathetic activity can lead to tachycardia, vasoconstriction, and cardiac arrythmias.
36
tachycardia and heart failure
tachycardia increases the workload of the heart, increasing oxygen demand and leads to cardiac ischemia and decreased inotropy. Cardiac ischemia and cardiomyopathy both contribute to worsening heart failure.
37
catecholamines (EPI and NE) and heart failure
prolonged exposure to sympathetic stimulation may lead to desensitization of beta adrenergic receptors without affecting the alpha adrenergic receptors. Even though circulating NE levels are increased in persons with heart failure, the lack of functioning beta adrenergic receptors in relation to alpha adrenergic receptors may lead to vasoconstriction and an increase in systemic vascular resistance.
38
Why is increased vascular resistance bad in heart failure?
Increased systemic vascular resistance causes an increase in cardiac afterload and ventricular wall stress, thus increasing myocardial oxygen consumption. Other effects include decreased renal perfusion and additional augmentation of the RAAS, which increases blood volume, as well as decreased blood flow to skin, muscle, and abdominal organs.
39
what is one of the most important effectos of lowered cardiac output in heart failure?
decreased renal blood flow and glomerular filtration rate which leads to sodium and water retention. with decreased renal blood flow, kidneys secrete more renin and circulating levels of angiotensin II increase as well.
40
Angiotensin II
generalized and excessive vasoconstriction
facilitates release of NE
inhibits reuptake of NE by sympathetic nervous system
stimulates Aldosterone
Increases ADH levels
41
Aldosterone
increases tubular reabsorption of sodium which results in water retention. aldosterone is metabolized in the liver, and so its levels are further increased when heart failure causes liver congestion.
42
ADH
vasoconstrictor
| water retention
43
fluid retention and heart failure
the progressive accumulation of fluid leads to ventricular dilation and increased wall tension. This increases oxygen demand and eventually outweighs the compensatory Frank-Starling mechanism, reducing inotropy, and exacerbating heart failure.
44
angiotensin II and aldosterone and the inflammatory response
stimulate cytokine production (TNF and IL-6)
attract inflammatory cells (neutrophils and macrophages)
activate macrophages at site of injury
stimulate growth of fibroblasts
stimulate synthesis of collagen fibers
---Atherosclerosis!!!!!
45
tissue plasminogen activator
t-PA released slowly from injured tissues and vascular endothelium converts plasminogen to plasmin which digests the fibrin strands, causing the clot to dissolve=CLOT DISSOLUTION
46
fibrinolysis
process by which a clot dissolves
47
tPA is used to treat what?
tPA is the first and only agent approved by the FDA for treatment of acute ischemic stroke. this treatment plan is called thrombolytic therapy. major risk is intracranial hemorrhage of the infarcted brain.
48
cardiac tamponade
compression of the heart due to accumulation of fluids, pus, or blood in the perocardial sac.
49
what causes cardiac tamponade
infection, neoplasms, bleeding
50
cardiac tamponade results in
increased intracardiac pressure, progressive limitation of ventricular diastolic filling, and reductions in stroke volume and cardiac output
51
pulsus paradoxus
a key diagnostic finding, an exaggeration of the normal variation in the sytemic arterial pulse volume with respiration. In cardiac tamponade, the left ventricle is compressed from within by movement of the interventricular septum and from the outside by fluid in the pericardium. this produces a marked decreased in left ventricular filling and left ventricular stroke volume output.
52
what indicates tamponade?
a decline in systolic pressure greater than 10 mm Hg during inspiration
53
treating tamponade
NSAIDS, colchicine, corticosteriods may minimize fluid accumulation
pericardiocentesis-removal of fluid
54
HDL cholesterol
```
high density lipoprotein
50% protein
the good cholesterol
reverse transport of cholesterol by carrying cholesterol from the tissues back to the liver for excretion
normal levels 40-60 mg/dL
```
55
apoproteins
control the interactions and ultimate metabolic fate of the lipoproteins. the major apoprotein for HDL is apoA-I
56
Research suggests that genetic defects in apoproteins may be involved in
hyperlipidemia and accelerated atherosclerosis
57
two sites of lipoprotein synthesis
small intestine
| liver-synthesizes and releases VLDL and HDL
58
ATP binding cassette transporter A class 1 (ABCA1)
specialized lipid transporter that promotes the movement of cholesterol from the tissues and to HDL
59
defects of ABCA1
Tangier Disease-accelerated atherosclerosis and little or no HDL
60
HDL inhibits
cellular uptake of LDL by reducing oxidation thereby preventing uptake of oxidized LDL by the scavenger receptors on macrophages
61
How to increases HDL?
regular exercise
moderate alcohol consumption
certain liquid medications
62
what decreases HDL?
smoking
| the metabolic syndrome
63
albumin
smallest of the plasma proteins
does not pass through the pores in the capillary wall therefore contributes to plasma osmotic pressure and maintenance of blood volume
serves as a carrier for certain substances and acts as a blood buffer
64
edema due to decreased capillary colloidal osmotic pressure is usually the result of
a lack of albumin due to liver failure (albumin is synthesized in the liver) or starvation, edema develops because there is a lack of amino acids for plasma protein synthesis
65
When can you lose plasma proteins?
In kidney diseases like glomerulonephritis, the glomerular capillaries become permeable to albumin and then large amounts of albumin are filtered out of the blood and lost in the urine--edema
burns, or large areas of damaged skin=loss of plamsa proteins--edema
66
albumin binds and transports
hormones (thyroid 15% T3, T4), fatty acids, bilirubin, and other anions
67
Thyroid hormone
increases the metabolism and protein synthesis in nearly all tissues of the body
necessary for brain development and growth in infants and small children
68
causes of heart failure
CAD
hypertension
dilated cardiomyopathy
valvular heart disease
69
sympathetic nervous system and heart rate
speeds it up
70
parasympathetic nervous system and heart rate
slows it down
71
stroke volume is a combination of
preload, afterload, and myocardial contractility
72
beta adrenergic receptors (EPI and NE=catecholamines bind here)
coupled with cAMP to open L-type calcium channels during inotropy to increase strength of cardiac contraction
73
digitalis
inhibits the sodium/calcium channel in the myocardium to increase inotropy because calcium builds up inside of the cells
74
Systolic Ventricular Dysfunction
myocardial contractility is impaired, leading to a decrease in the ejection franction and cardiac output.
75
Diastolic Ventricular Dysfunction
is characterized by a normal ejection fraction but impaired diastolic ventricular relaxation, leading to a decrease in ventricular filling that ultimately causes a decrease in preload, stroke volume, and cardiac output.
76
cor pulmonale
High blood pressure in the arteries of the lungs is called pulmonary hypertension. The right side of the heart has a harder time pumping blood to the lungs when this happens. If this high pressure continues, it puts a strain on the right side of the heart, leading to cor pulmonale.
77
emphysema
loss of lung elasticity and abnormal enlargement of the air spaces distal to the terminal bronchioles, with destruction of the alveolar walls and capillary beds. This enlargement of the air sacs leads to hyperinflation of the lungs and produces an increased in total lung capacity (TLC).
78
what causes emphysema?
smoking
inherited deficiency of alpha 1 antitrypsin an antiprotesase enzyme that protects the long from injury.
Emphysema is thought to result from the breakdown of elastin (by the enzyme elastase) and other alveolar wall components by enzymes called proteases that digest proteins. These proteases are released from neutrophils, macrophages, and other inflammatory cells. When you smoke (or other irritants) then you cause an influx of inflammatory cells to travel to the lungs, they releases their protein eating enzymes (the proteases) and the enzymes eat the elastic aspect of the lung wall.
Besides smoking, the other major known cause of emphysema is alpha-1 antitrypsin deficiency. However, this is a minor cause of emphysema, compared to smoking.
Alpha-1 antitrypsin (AAT) is a natural protein circulating in our blood. Its main function is to keep white blood cells from damaging normal tissues. White blood cells contain destructive substances they use to fight infections.
Some people -- perhaps 100,000 people in the U.S. -- have a genetic condition that makes them deficient in alpha-1 antitrypsin. Deficient levels of the AAT protein in the blood allow normal white blood cells to continuously damage lung tissue. If people with AAT deficiency smoke, the damage is even worse.
79
inherited deficiency of alpha1 antitrypsin
autosomal recessive trait
determined by PI (protein inhibitor) genes
most serious gene mutation is the PIZ gene where you have only 15-20% the alpha 1 antitrypsin you are supposed to.
In its absence, neutrophil elastase is free to break down elastin, which contributes to the elasticity of the lungs, resulting in respiratory complications such as emphysema, or COPD (chronic obstructive pulmonary disease) in adults and cirrhosis in adults or children.
80
panacinar emphysema
type of emphysema most often seen with the deficiency of alpha1 antitrypsin. produces initial involvementof the peripheral alveoli and later extends to involve the more central bronchioles. Most often in the lower parts of the lung
81
centriacinar or centrilobular emphysema
most often seen in the upper part of the lung.
Affects the bronchioles in the central part of the respiratory lobule, with initial preservation of the alveolar ducts and sacs. Most common form of emphysema and most often seen in male smokers
82
addisons disease
primary adrenal insufficiency
adrenal cortical hormones are deficient and ACTH levels are elevated due to lack of feedback inhibition
all layers of adrenal cortex are destroyed
83
addisons disease manifestations
hyponatremia
loss of extracellular fluid
decreased CO
hyperkalemia
orthostatic hypotension
dehydration
weakness
fatigue
cardiovascular collapse and potential shock
poor tolerance to stress-hypoglycemia, lethargy, weakness, fever, anorexia, nausea, vomiting, weight loss
elevated ACTH causes hyperpigmentation
84
immunizations
active immunity
| memory B and T lymphocytes respond to subsequent exposure to antigens
85
Rheumatioid Arthrities
a chronic systemic inflammatory disease with bilateral involvement of synovial or diarthrodial joints
86
pathophysiology of RA
synovial cells line the joint. Inflammatory cells accumulate and cause angiogenesis and pannus to form, which proceed to cover the articular cartilage and isolate it from its nutritional synovial fluid.
87
pannus
a feature of RA that differentiates it from other forms of inflammatory arthritis. The inflammatory cells found in the pannus have a destructive effect on the adjacent cartilage and bone. Pannus develops over the joint margins leading to reduced joint motion and the possibility of ankylosis.
88
cellular components of RA
Activated T cell mediated immune response
cytokines released (TNF, IL-1)
Antibody formation
89
MHC and HLA in RA
```
MHC genes (major histocompatibility complex
HLA human leukocyte antigen on MHC class II molecules with a specific set of HLA DR alleles (DR4, DR1, DR10, DR14) These allesles are thought to form a shared epitope in the hypervariable segemnt of the HLA-DRB1 gene, which forms a rheumatoid pocket on the HLA molecule. the binding properties of this pocket influence the types of peptides that can be bound by the RA-associated HLA-DR molecules, therby affecting the immune response
```
90
rheumatoid factor
Ig RF reacts with a fragment of Ig to form immune complexes in persons with RA (Ig RF + IgG. These immune complexes attract neutrophils, macrophages, and lymphocytes to phagocytize them and while they are doing so, they release lysosomal enzymes that destroy joint cartilage. The inflammatory response that follows attracts additional inflammatory cells, setting into motion a chain of events that perpetuates the conditon. as the inflammatory process progresses, synovial cells and subsynovial tissues undergo reactive hyperplasic. Vasodilation and increased blood flow cause warmth and redness. Joint swelling occurs as a result of the increased capillary permeability that accompanies the inflammatory process.
91
clinical manifestations RA
```
fatigue
anorexia
weight loss
generalized achiness and stiffness
joint manifestations are symmetric and polyarticular. Any diarthridal joint can be affected.
```
92
four characteristics must be present to diagnose RA
1. morning stiffness for at least 1 hour at least 6 weeks
2. simultaneous swelling of thee or more joints for at least 6 weeks
3. Swelling of weist, metacapophalangeal, or proximal interphalangeal joints for 6 or more weeks
4. symmetric joint swelling for 6 or more weeks
5. Rheumatoid nodules
6. serum rheumatiod factor identified by a method that is positive in less than 5% of norma subjects
7. radiographic changes typical of theumatoid arthritis on hand or wrist radiographs
93
What antibody presence helps diagnose RA?
Anti-cyclic citrullinated peptide (CCP) antibodies
| citrulline-containing proteins may serve as specific targets for the IgG antibody response in RA.
94
Multiple Sclerosis
inflammation and selective destruction of CNS myelin
| HLA-DR2 human leukocyte antigen haplotype
95
Interleukin 12
responsible for differentiation of T cells; overproduction of IL12 is what causes inflammatory response in MS
96
oligodendrodytes
built myelin sheath around neuron affected by MS
97
Insulin
acts to increase protein and lipid synthesis, promotes glucose storage, and inhibits gluconeogenesis or the building of glucose from amino acids
98
a preventative measure to decrease the risk of developing rheumatic heart disease
is prompt diagnosis of streptococcal infections with a throat culture. Rheumatic heart disease is commonly caused by strptococcal infections.
99
serum phenylalanine test
a procedure performed on a newborn to decrease the risk of mental retardation and impaired neurological development. Newborn infants are routinely screened within 12 hours of birth to detect high levels of serum phyenylalnine that could cause irresversible mental retardation.
100
cardiogenic shock
decreased CO, hypotension, hypoperfusion, tissue hypoxia despite adequate inravascular volume. Decreased CO caused by decreased inotropy, increased afterload, or excessive preload.
myocardial damage (infarction, contusion)
sustained arrythmias
acute valve damage, ventricular septal defect
Cardiac surgery
CAD
cardiomyopathy
101
hypovolemic shock
```
caused by decreased blood volume
loss of whole blood (hemorrhage)
loss of plasma (burns)
loss of extracellular fluid (vomiting, diarrhea, dehydration)
Internal hemorrhage
third spacing
```
102
Obstructive shock-elevated right heart pressure due to impaired right ventricular fuction
caused by obstruction of blood flow through circulatory system
inability of the heart to fill properly (cardiac tamponade)
Obstruction to outflow from the heart (pulmonary embolus, cardiac myxoma, pneumothorax, or dissecting aneurysm)
103
Distributive shock
excessive vasodilation with maldistribution of blood flow
loss of sympathetic vasomotor tone (neurogenic shock)
presence of vasodilating substances in the blood (anaphylatic shock)
presence of inflammatory mediators (septic shock)
104
cardiac tamponade
inability of heart to fill properly
| obstructive shock
105
neurogenic shock
loss of sympathetic vasomotor tone
| distributive shock
106
anaphylatic shock
presence of vasodilating substances in the blood
| distributive shock
107
septic shock
presence of inflammatory mediators
| distributive shock
108
compensatory mechanisms to circulatory shock
sympathetic and renin systems are designed to maintain cardiac output and blood pressure
109
stimulation of alpha receptors (SNS)
vasoconstriction
110
stimulation of beta 1 receptors (SNS)
increase heart rate and inotropy
111
stimulation of beta 2 receptors (SNS)
vasodilation of skeletal muscle and relaxation of bronchioles
112
What occurs in most types of shock?
Increased heart rate and vasoCONSTRICTION
due to EPI and NE released by SNS to activate both the alpha and the beta receptors
-increased RENIN release leading to increased angiotensin II which augments vasCONSTRICTION and leads to ALDOSTERONE mediated increase in sodium and water retention by the kidneys
113
Why are these compensatory mechanisms bad in the long term?
intense vasocontriction causes a decrease in tissue perfusion and hypoxemia. This impairs cellular metabolism, and vasoactive inflammatory mediators like histamine are released, production of oxygen free radicals is increased, and excessive lactic acid and hydrogen ions result in intracellular acidity. each of these factors promote cellular dysfunction or death.
114
acs (acute coronary syndrome) ECG changes
ST elevation, prolongation of Q wave, inverted T wave
115
treatment regimens for ACS
oxygen, aspirin, nitrates, pain medications, antiplatelet and anticoagulant therapy, beta blockers and ACE inhibitors
116
persons with ECG evidence of infarction should receive immediate
reperfusion therapy with a thrombolytic agent or percutaneous coronary intervention (PCI)
117
Nitroglycerin
```
vasodilator
relieve coronary pain
decreases venous return (reduce preload)
and arterial blood pressure (reduce afterload)
thereby reducing oxygen consumption
```
118
beta blockers
block the beta receptors stimulated by the SNS
blocking these receptor sites functions to SLOW HR and inotropy thereby reducing myocardial oxygen demands. Beta blockers also function to lower blood pressure. Beta blockers also resting myocardial membrane potentials and may decrease life-threatening ventricular arrythmias
119
when dont you give beta blockers?
```
cocaine related STEMI - accentuate coronary spasm
bradycardia
hypotension
mod-severe left ventricular failure
shock
2-3rd degree heart block
```
120
aspirin
anti-platelet aggregation
inhibits synthesis of prostaglandin thromboxane A2
promotes reperfusion and reduce the likelihood of rethrombosis
121
fibrinolytic therapy
dissolve blood and platelet closts and are used to reduce mortality, limit infarct size, encourage infarct healing and myocardial remodeling, and reduce the potential for life-threatening arrythmias.
interact with plasminogen to generate plasmin, which lyses fibrin clots and digests clotting factors V and VIII, prothrombin, and fibrinogen. =tPA tenecteplase
primary complication of fibronlytic therapy is intracranial hemorrhage
122
cardiogenic shock may lead to
systemic inflammatory response syndrom evidenced by elevated WBC, increased temperature, and release of inflammatory markers such as CRP
123
compensatory mechanisms for hypovolemic shock
tachycardia, increased inotropy, vasoconstriction, fluid absorption from interstitial spaces, conservation of sodium and water by the kidneys, and thirst
124
how do the capillaries respond to loss of blood volume?
when there i a loss of vascular volume, capillary pressures decrease and water is drawn into the vascular compartment from the interstitial spaces.
125
How do the kidneys respond to low blood volume?
a decrease in renal blood flow and GFR actives the RAAS, which produces an increase in sodium reabsorption by the kidneys. The decrease in blood volume also stimulates centers in the hypothalamus that regulate ADH release and thirst. ADH constricts peripheral arteries and veins and greatly increases water retention by the kidneys.
126
hypovolemic shock signs and symptoms
```
thirst
increased heart rate (weak and thready)
cool, clammy skin
decreased arterial bp
decreased urine output
changes in mentation
```
127
distributive or vasodilatory shock aka normovolemic shock
the capacity f the vascular compartment expands to the extent that a normal volume of blood does not fill the circulatory system.
128
2 causes of lost vascular tone
decrease in sympathetic control of vasomotor tone
release of excessive vasodilator substances
3. vessel damage resulting from prolonged and severe hypotension due to hemorrhage
129
3 shock states under distributive shock
neurogenic shock
anaphylactic shock
septic shock
130
neurogenic shock
decreased sympathetic control of blood vessel tone due to a defect in the vasomotor center the in brain stem or the sympathetic outflow to the blood vessels.
spinal shock
131
how can the output from the vasomotor center be interrupted?
brain injury, depressant action of drugs, general anesthesia, hypoxia, lack of glucose (insulin reaction)
132
neurgenic shock manifestations
SLOW heart rate***
| warm dry skin
133
anaphylactic shock
most severe systemic allergic reaction
immunologically mediated reaction in which vasodilator substances (histamine) are released into the blood.
increased vasodilation, increased cap perm,
laryngeal edema, bronchospasm, circulatory collapse, contraction of GI and uterine smooth muscle, urticaria (hives) and angioedema
134
epinephrine in anaphylactic shock
epinephrine constricts blood vessels and relaxes the smooth muscle in bronchioles, thus restoring cardiac and respiratory function
135
sepsis
suspected or proven infection
plus a systemic inflammatory response (fever, tachycardia, tachypnea, elevated WBC, altered mental state, hyperglycemia without diabetes)
136
severe sepsis
sepsis+organ dysfunction (hypotension, hypoxemia (low O2 in blood), oliguria, metabolic acidosis, thrombocytopenia (low platelets), or obtundation (altered LOC))
137
septic shock
severe sepsis + hypotension despite fluid resuscitation
138
mechanism of septic shock
TLRs (toll like receptors) bind to infectious agent leads to the release of proinflammatory mediators such as cytokines, recruitment of neutrophils and moncytes, involvement of neuroendocrine reflexes, and activation of complement, coagulation, and fibrinolytic systems.
139
proinflammatory mediators TNF-alpha and IL1 (activated by TLRs)
leukocyte adhesion, local inflammation, neutrophil activation, suppression of erythropoiesis, generation of fever, tachycardia, lactic acidosis, ventilation-perfusion abnormalities, and other signs of sepsis.
140
activated neutrophils
kill bad microorganisms, but also kill endothelium by releasing mediators that increase vascular permeability. in addition, activated endothelial cells release nitric oxide, a potent vasodilator that acts as a key mediator of septic shock
141
sepsis and procoagulation and anticoagulation balance
increase procoagulation
decrease anticoagulation
lipopolysaccharides on the surface of microorganisms stimulates endothelial cells lining blood vessels to increase their production of tissue factor, thus activating coagulation. Fibrinogen is then converted to fibrin leading to the formation of microvascular thrombi that further amplify tissue injury.
142
manifestations of septic shock
hypotension, warm flushed skin, decreased vascular resistance***, hypovolemia, altered behavior, fever, increased leukocytes, tissue hypoxia, metabolic acidosis
143
5 major complications of severe shock
```
pulmonary injury-ARDS
acute renal failure
GI ulceration
disseminated intravascular coagulation DIC
multiple organ dysfunction sydrome
```
144
ARDS
can occur bc of shock
| fluid and plasma protein leak into interstitium and alveolar spaces--ATELECTASIS
145
disseminated intravascular coagulation DIC
widespread activation of the coagulation system with resultant formation of fibrin clots (bc of increased thrombin) and thrombotic occlusion of small and midsized vessels.
146
which organ is affected most in right sided failure?
liver
147
intra-aortic balloon pump for cardiogenic shock
aka counterpulsation, enhances coronary and systemic perfusion yet decreases afterload and myocardial oxygen demands
148
diabetes insipidus
deficiency or decreased response to ADH
excrete large volumes of urine
excessive thirst
hypertonic dehydration and increased serum osmolality
149
two types of DI
Neurogenic or Central Diabetes Insipidus-defect in the synthesis or release of ADH
Nephrogenic DI-kidneys don't respond to ADH
150
neurogenic DI causes
head injury
| surgery near the hypothalamohypophysical tract
151
Nephrogenic DI
genetic train affecting the V2 receptor that binds ADH, or the aquaporin-2 protein that forms the water channels in the collecting tubules. lithium and elctrolyte disorders are thought to interfere with the postreceptor actions of ADH on the permeability of the collecting ducts
152
cholelithiases clinical manifestations
Epigastric & upper right quadrant pain radiating to mid-upper back
Intolerance to fatty foods
Heartburn, flatulence, epigastric discomfort
Jaundice (stone located in the common bile duct)
Food intolerances (fats)
Biliary colic (pain) cause by the lodging of gallstone in cystic or common duct
Pain intermittent or steady
153
cholelithiases problem foods
fatty foods
salt
alcohol
need bile to break down fat, so when we take out gall bladder, watch fat intake
154
large amounts of iodine (ingestion of kelp tablets, or iodide containing cough syrups, or administration of iodide containing radiographic contrast media or the cardiac drug amiodarone, which contains 75 mg of iodine per 200 mg tablet) can block thyroid hormone production and cause
goiter
155
iodine deficiency
can cause goiter and hypothyroidism
156
Hashimoto thyroidititis
an automimmune disorder in which the thyroid gland may be totally destroyed by an immunologic process is the major cause of goiter and hypothyroidism in children and adults
157
hyperthyroidism-graves disease
goiter too. too much thyroid hormone accumulates-treat with I-131 to kill the thyroid gland!!
158
cholelithiasis
gallstones; caused by precipitation of substances in bile, mainly cholesterol and bilirubin.
159
three factors contribute to the formation of gall stones
abnormalities in the composition of bile
stasis of bile
inflammation of the gall bladder
160
cholesterol stone formation
linked to obesity, oral contraceptive, and is more prevalent in women. All these factors cause the LIVER to EXCRETE more CHOLESTEROL into bile
161
synthroid
synthetic T4. given to supplement thyroid function in hypothyroidism
162
iodine + T3
T4=thyroid hormone
163
Hypothyroidism
```
slow metabolic functions
cold
overweight
myxedema-third spacing, shock, coma
Hashimotos
goiter
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164
Hyperthyroidism
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hot
fast metabolism
thin arms and legs
goiter
exopthalmos
Graves Disease
THERMOGENICS discontinued medication that speeds up body functions so you burn fat while not working out. BAD for hyperthyroidism, made hypothyroidism people feel more normal-caused thyroid cancer though.
```
165
intra-aortic balloon pump
treatment for cardiogenic shock
aka counterpulsation
enhances coronary and systemic perfusion
decreases afterload and myocardial oxygen demands
the device pumps in synchrony with the heart, consists of a 10 inch balloon that is inserted through a catheter into the descending aorta. The balloon is timed to inflate during ventricular diastole and deflate just before ventricular systole. The diastolic inflation creates a pressure wave in the ascending aorta that increases coronary artery blood flow and a less intense wave in the lower aorta that enhances organ perfusion. The abrupt balloon deflation at the onset of systole results in a displacement of blood volume that lowers the resistance to ejection of blood from the left ventricle. Thus, the heart's pumping efficiency is increased and myocardial oxygen consumption is decreased.
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third degree heart block
Complete AV block. No atrial impulses pass from the SA through the AV node. Both the atria AND ventricles generate their own rhythm. NO BUENO.
NOT A SHOCKABLE RHYTHM = MUST USE A PACEMAKER
167
stemi
ST-elevation is an abnormal finding on the electrocardiogram of a heart attack patient.)
It is a profoundly life-threatening medical emergency and usually associated with atherosclerosis
Coronary artery is completely blocked off by the blood clot, and as a result virtually all the heart muscle being supplied by the affected artery starts to die
168
nstemi
Occurs when the blockage in the coronary artery is not complete, so that a relatively small proportion of heart muscle is becoming damaged
It is still an MI and still taken seriously
169
complications of diabetes mellitus
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1)Diabetic ketoacidosis
Hyperglycemia (blood glucose levels >250 mg/dL)
Ketonemia / ketonuria
Hyperkalemia
Metabolic acidosis (Low pH 600 mg/dL)
Hyperosmolarity (plasma osmolarity >310 mOsm/L)
Dehydration
The absence of ketoacidosis
Depression of the sensorium
```
3)Hypoglycemia
Blood glucose level <70 mg/dL (ADA)
4)Microvascular complications
Neuropathy, nephropathy, retinopathy
Foot ulceration
5)Macrovascular complications
Cardiovascular
Stroke
170
General Adaptation Syndrome
1) Alarm Stage
2) Resistance Stage
3) Exhaustion stage
171
Alarm stage
first stage of GAS
| Stimulation of SNS and HPA axis (hypothalamic-pituitary-adrenal) resulting the in release of catecholamines and cortisol
172
triad in GAS
adrenal enlargement
thymic atrophy
gastric ulcers
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dysentery
Dysentery is bloody diarrhoea, i.e. any diarrhoeal episode in which the loose or watery stools contain visible red blood. Dysentery is most often caused by Shigella species (bacillary dysentery) or Entamoeba histolytica (amoebic dysentery).
174
salivary amylase
Amylase digests starch by catalyzing hydrolysis, which is splitting by the addition of a water molecule. Therefore starch plus water becomes maltose (which is equivalent to two joined glucose molecules). Body temperature is the optimal heat for the best reaction of amylase.
175
benign prostatic hypertrophy
characterized by proliferation of the cellular elements of the prostate. Chronic bladder outlet obstruction (BOO) secondary to BPH may lead to urinary retention, renal insufficiency, recurrent urinary tract infections, gross hematuria, and bladder calculi.
176
benign prostatic hypertrophy
age related, non malignant enlargement of the prostate gland. forms large, discrete lesions in the periurethral region of the prostate
177
DHT (dihydrotestosterone)
the biologically active metabolite of testosterone is thought to be the ultimate mediator of prostatic hyperplasia, with estrogen serving to sensitize the prostatic tissue to the growth-producing effects of DHT. Free plasma testosterone enters prostatic cells, where at least 90% is converted into DHT by the action of 5alpha-reductase. this is why we use 5alpha reductase inhibitors to treat BPH.
178
how does estrogen add to the development of BPH?
| Benign Prostatic Hypertrophy
a relative increase in estrogen levels that occurs with aging may facilitate the action of androgens in the prostate despite a decline in testicular output of testosterone.
179
BPH symptoms
weak urinary stream
postvoid dribbling
frequency of urination
nocturia
180
how do we treat BPH?
5alpha reductase inhibitor-stop conversion of testosterone to DHT
alpha adrenergic receptor blockers as those are the main receptors for the smooth muscle component of the prostate.
181
clinical significance of BPH
tends to compress the urethra and cause partial or complete obstruction of urinary outflow
182
intermittent claudication-pain with walking
the primary symptom of PAD and chronic obstructive arterial disease (atherosclerosis)
typically, patients complain of calf pain bc the gastrocnemius has the highest oxygen consumption of any muscle group in the leg when walking.
183
peripheral artery disease (PAD)
PAD is a narrowing of the peripheral arteries, most commonly in the arteries of the pelvis and legs due to atherosclerosis
184
Jaundice (aka icterus)
a yellowish discoloration of skin and deep tissues resultant of high levels of bilirubin in the blood (>2-2.5mg/dL)
185
4 major causes of jaundice
1) excessive destruction of RBCs
2) impaired uptake of bilirubin by the liver
3) decreased conjunction of bilirubin
4) obstruction of bile flow in the canaliculi of the hepatic lobules or in the intrahepatic or extrahepatic bile ducts
186
anatomic classifications of jaundice
prehepatic-excessive hemolysis of RBCs
intrahepatic
posthepatic
187
when is conjugation of bilirubin impaired?
whenever liver cells are damaged, when transport into liver cells becomes deficient, or when the enzymes needed to conjugate the bile are lacking
188
which liver diseases are most common causes of intrahepatic jaundice?
hepatitis and cirrhosis
189
cholestatic jaundice (posthepatic jaundice)
occurs when the bile flow is obstructed between the liver and the intestine-gallstone could be the cause here
190
Key liver enzymes
ALT
AST
in most cases of liver damage, these #s rise
191
GGT
thought to function in the transport of amino acids and peptides into liver cells- a sensitive indicator of hepatobiliary disease. Measurement of GGT may be helpful in diagnosing alcohol abuse
192
Factors V, VII, IX, X, prothrombin, and fibrinogen
are synthesized by the liver and their decline in liver disease contributes to bleeding disorders
193
treatment for acute pancreatitis
directed at pain relief
put the pancreas at rest by withholding oral foods and fluids, restore lost plasma volume. Gastric suctioning is initiated to rest the pancreas and teat distention of the bowel
194
which lab studies should you anticipate being ordered for a patient who is suspected of having pancreatitis?
serum amylase and lipase
195
which substance has been shown to cause partial obstruction of the sphincter of the pancreas?
alcohol
196
what long-term effect can chronic pancreatitis have?
diabetes and malabsorption
197
what symptoms are seen in patients with suspected pancreatitis?
tachycardia
fever
epigastric pain
tenderness
198
signs and symptoms of jaundice
confusion, slurred speech, sleepy, flapping arms and hands, angry, screaming, personality changes, convulsions, coma, death
We give LACTULOSE!
199
nitrogenous wastes
ammonia, urea, uric acid
200
Primary Immune Response
b cells are activated to proliferate and differenetiate into antibody secreting plasma cells. Some do not differentiate-instead, they become memory b cells
201
acute renal failure labs
Normal blood contains 7-20 mg/dl of urea. If your BUN is more than 20 mg/dL, your kidneys may not be working at full strength
Creatinine is a waste product in the blood created by the normal metabolism of muscle cells. Healthy kidneys take creatinine out of the blood and remove it into the urine to leave the body. When the kidneys are not working well, creatinine builds up in the blood. If the kidneys lose their ability to filter blood (GFR decreases) more creatinine will accumulate and serum creatinine will rise. As a result, creatinine is an indirect marker of glomerular filtration rate (GFR) or how well the kidneys work. A creatinine level of greater than 1.2 for women and greater than 1.4 for men may be an early sign that the kidneys are not working properly.
The normal value for GFR is 90 ml/min or above. A GFR below 60ml/min is a sign that kidneys are not working properly. A GFR below 15 ml/min indicates that a treatment for kidney failure, such as dialysis or transplant will be needed.
Healthy kidneys take wastes out of the blood but leave protein. Impaired kidneys may fail to separate a blood protein called albumin from the wastes. At first, only a small amount of protein that is too small to be measured with a standard dipstick may leak into the urine. This condition is known as microalbuminuria. This is how the test is read:
Less than 30 mg/L is normal
Greater than 30 mg/L but less than 300 mg/L is called microalbuminuria
Greater than 300 mg/L is called macroalbuminuria
Urine Protein Test
As kidney function worsens, the amount of albumin and other proteins in the urine often increases, and the condition is called proteinuria. Your doctor may test for protein using a dipstick in a small sample of your urine taken in the doctor's office. The color of the dipstick indicates the presence or absence of proteinuria. This test should be negative.
202
azotemia
accumulation of nitrogenous wastes in blood-indicates acute renal failure
203
fracture complications
delayed union
malunion
nonunion
injury from bone fragments
pressure from swelling and hemorrhage (fracture blisters, compartment syndrome)
involvement of nerve fibers (complex regional pain syndrome)
development of venous thromboembolism and fat embolism syndrome
204
fraction blisters
represent areas of epidermal necrosis with separation of epidermis from the underlying dermis by dema fluid. they occur when the intercompartmental pressure is TOO HIGH to be relieved by normal means.
205
compartment syndrome
increased pressure within a limited space that compromises the circulation and function of the tissues in the space. if the pressure gets too high, the muscle and nerve cells may die.
206
TNF-alpha
secreted by macrophages and mast cells and acts to induce fever
207
Neutrophils
are the predominant phagocytes in the early inflammatory site
208
interleukins
are biochemical messengers produced by macrophages and lymphocytes in response to a pathogen
209
C5b
The complement factor that causes pores to form in the bacterial membrane
210
Complex Regional Pain Syndrome
soft tissue injuries of musculoskeletal injuries that cause pain out of proportion to the injury and autonomic nervous system dysfunction manifested by hyperhidrosis (increased sweating) and vasomotor instability (either flushed and warm or cold and pale)
211
Thromboemboli
pulmonary embolism or deep vein thrombosis
212
fat embolism syndrome (FES)
presence of fat droplets in the small blood vessels of the lung or other organs after a long bone fracture or other major trauma. The fat emboli are thought to be released from th bone marrow or adipose tissue at the fracture site into the venous system through torn veins.
FES features: respiratory failure, cerebral dysfunction, skin and mucosal petechiae.
213
craniotomy
A craniotomy is a surgical operation in which a bone flap is temporarily removed from the skull to access the brain. Craniotomies are often a critical operation performed on patients suffering from brain lesions or traumatic brain injury (TBI), and can also allow doctors to surgically implant deep brain stimulators for the treatment of Parkinson's disease, epilepsy and cerebellar tremor. The procedure is also widely used in neuroscience for extracellular recording, brain imaging, and for neurological manipulations such as electrical stimulation and chemical titration.
214
where is pain integrated and modulated in the brain?
Thalamus and somatosensory cortex
215
substance P and Glutamate
nocioceptive pain stimulation releases these substances to perpetuate pain response
216
radiation
increases malignant epitheliomas of the skin and leukemia
217
loop of henle
plays an important role in urine concentration
establishes a high concentration of osmotically active particles in the interstitium surrounding the medullary collecting tubules where the ADH exerts its effect. Loop of henle always absorbs more sodium and chloride than water.
218
How is T cell Differentiation skewed in asthma patients?
CD4+T-lymphocytes differentiate into TH2 cells more than TH1 cells. TH2 cells react to allergens and incite B cells to differentiate into IgE producing plasma cells. These IgE release growth factors to mast cells and recruit and activate eosinophils (inflammatory cells)
219
Eosinophils and Neutrophils in Asthma
contribute to airway remodeling by increasing proliferation of fibroblasts, increased production of extracellular matrix glycoproteins, and mucous cell hyperplasia
220
TNF-alpha, IL4, IL5 and Asthma
TNF-alpha is released from mast cells and acts to increase the migration and activation of inflammatory cells (eosinophils and neutrophils) which damage bronchial epithelial and smooth muscle cells.
221
stimulation of parasympathetic receptors causes what in asthma
bronchospasms
222
increased vascular permeability causes what is asthma
mucosal edema
223
How do you inhibit the acute asthma response?
use bronchodilators such as Beta 2 adrenergic agonists
| do not use corticosteroids
224
anticholinergic medications treat asthma
block the postganglionic efferent vagal pathways that cause vasoconstriction. they produce bronchodilation by direct action on the large airways and do not change the composition or viscosity of the bronchial mucus
225
corticosteriods and asthma
use to treat the inflammation of the late phase response
226
AV node
provides the only connection between the atrial and ventricular conduction systems. The atria and ventricles would beat independently of each other if the transmission of impulses through the AV node were blocked.
227
AV node rate
40-60 times/minute. PR segment represents the delay in the AV node while the ventricles fill with blood
228
deep venous thrombosis
thrombus in a vein and the accompanying inflammatory response in the vessel wall. DVT is most commonly in the lower extremities
229
where do most postoperative thrombi arise? why are they a concern?
in the soleal sinuses or the large veins draining the gastrocnemius muscles. If left untreated, they may extend to larger, more proximal veins with an increased risk of pulmonary emboli
230
Triad associated with DVT
stasis of blood
increased blood coagulability
vessel wall injury
231
Thrombosis can be caused by inherited or acquired deficiencies of certain plasma proteins that normally inhibit thrombus formation such as (3)
antithrombin III
protein C
protein S
232
Most common inherited risk factors for clotting:
factor V Leiden and prothrombin gene mutations
233
plasma d dimer assessment
a positive result indicates presence of thrombosis and is often used to diagnose DIC
234
pulmonary embolism
a blood borne substance lodges in a branch of the pulmonary artery and obstructs blood flow.
235
result of pulmonary embolus
```
reflex bronchoconstriction
wasted ventilation
impaired gas exchange
loss of alveolar surfactant
pulmonary hypertension
right sided heart failure
```
236
Exophthalmos
hyperthyroidism
237
ammonia buffer system
acts to regulate pH by eliminating H+ in urine. Acts primarily inthe proximal convuluted tubule, but ammonia can sub for K+ in the triple transport channel in the loop of henle
238
production, transport, and excretion of ammonium by the kidney(NH4)
glutamate is metabolized in the proximal tubule to produce two NH4+ and two HCO3-
NH4 secreted to tubular fluid, HCO3- returned to circulation
NH4 gets reabsorbed as NH3 and NH4, NH3 diffuses into collecting tubule and grabs H+ to form NH4 again and is excreted in urine. For every NH4 excreted in urine, one HCO3- is added back to circulation
239
Pancreatic secretions
break down dietary proteins: trypsin, chymotrypsin, carboxypolypeptidase, ribomuclease, and deoxyribonuclease
break down starch - pancreatic amylase
hydrolyze neutral fats into glycerol and fatty acids-lipases
240
acinar cells of pancreas
secrete trypsin inhibitor-keeps trypsin inactive
trypsin activates the other enzymes, if they are activated before they reach the small intestine, they will eat the tissue of the pancreas itself!
241
acute pancreatitis
reversible inflammatory process of the pancreatic acini brought about by premature activation of pancreatic enzymes leading to autodigestion of pancreatic tissues
242
Main causes of acute pancreatitis
```
gallstones
alcohol abuse
hyperlipidemia
hypercalcemia
thiazide diuretics
```
243
diagnosis of acute pancreatitis
serum amylase and lipase
increased WBC
hyperglycemia
elevated serum bilirubin
244
pancreatitis
epigastric and upper left quadrant pain
| attacks precipitated by alcohol abuse or overeating
245
hematocrit
measures the % RBC in 100 mL of plasma
men 40-50%
women 37-47%
246
Normal Hb
female 12-16 g/dL
| males 12-18 g/dL
247
HIV
Infects T helper cells, macrophages & B cells
| Depletion of T helper cells occurs more readily than other body cells and causes the immunodeficiency
248
HIV and CD4
HIV is completely dependent upon CD4 cells for replication and survival.
Actual diagnosis of AIDS is made when the CD4 count falls below 200 cells/cmm or when an AIDS-defining opportunistic condition is diagnosed.
249
Normal Platelet
150,000-400,000mm3
250
Amyotrophic Lateral Sclerosis (ALS) Lou Gehrig disease
ALS selectively affects motor function
ALS affects motor neurons in three locations:
anterior horn cells (LMNs)
motor nuclei of brain stem, hypoglossal nuclei
UMNs of cerebral cortex
this disease is more extensive in the distal parts of the affected tracts in the lower spinal cord rather than the proximal parts, suggesting that affected neurons first undergo degeneration at their distal terminals and the disease proceeds in a centripetal direction until ultimately the parent nerve cell dies. The entire sensory system remains intact:control and coordination of movement, intellect, ocular motility and sacral spinal cord.
251
a gene for a subset of familial ALS has been mapped to
SOD1 on chromosome 21
252
Riluzole
treats ALS by decreasing glutamate accumulation
| glutamate exitotoxicity is a suspected cause of ALS
253
parkinson disease
degenerative disorder of basal ganglia function that results in variable combinations of tremor, rigidity, and bradykinesia. Dopamine depletion-degeneration of nigrostriatal dopamine neurons
254
substantia nigra
produces dopamine (parkinson disease)
255
gene mutations associated with Parkinson Disease
lewey bodies-alpha-synuclein
parkin protein
UCH-L1
256
levodopa
a precursor of dopamine that can cross the BBB has yielded significant improvement of clinical symptoms of parkinson disease ( converted to dopamine in the brain by dopa decarboxylase)
257
erythropoeitin
90% made in the kidneys, 10% made in liver
decreased Oxygen content of blood is sensed by peritubular cells in the kidneys which then produce erythropoeitin to stimulate RBC production
258
erythropoeitin and renal failure
not enough erythropoeitin to make rbc in bone marrow
259
Chronic Kidney Disease (CKD)
progressive decline in kidney function due to the permanent loss of nephrons
GFR > 60mL/min/1.73m2 for three months or longer
260
Extra cellular fluid volume depletion
can cause CKD
261
Kidney Failure
GFR > 15 mL/min/1.73m2
| uremia
262
Normal GFR
120-130mL/mn/1.73m2
263
How is GFR usually estimated in clinical practice?
serum creatinine concentration
264
albuminuria
key tool for measuring nephron injury and repair
| DM or hypertension can cause high levels of albumin in urine and high albumin in urine indicates CKD
265
Manifestations of CKD
```
hypertension
hyperkalemia
edema
pericarditis
heart failure
anemia
acidosis
hypocalcemia
hyperparathyroidism
```
266
Kidneys and vit D
Kidneys convert vit D to its active form called calcitriol. Calcitriol suppresses PTH secretion
reduced levels of calcitriol mean elevated PTH which means increased calcium resorption from bone-leads to osteodystrophies
Reduced calcitriol also means less calcium absorption from the GI tract
Vit D regulates osteoblast differentitation, thereby affecting bone replacement.
267
retroperitoneal bleeding
```
anticoagulation
a ruptured aortic aneurysm
a ruptured renal aneurysm
acute pancreatitis
malignancy
```
268
turners sign
predicts acute pancreatitis attack
269
good pasture syndrome
glomerulonephritis that is caused by antibodies to the glomerular basement membrane. The anti-GBM antibodies cross react with the pulmonary alveolar basement membrane to produce the syndrome of pulmonary hemmorhage associated with renal failure.
270
toxicities of loop diuretics (furosemide (sulfa) and ethacrynic acid)
```
OHDANG
ototoxicity
hypokalemia
dehydration
allergy
nephritits
gout
```
271
how loop diuretic works
```
increase sodium secretion, water follows
kill K+ gradient which decreases the reabsorption of K+, Mg 2+ and Ca2+
Potential hypokalemia
hyponatremia
metabolic alkalosis
BP is low to normal
result: lose Na, K, Cl, Ca, Mg
```
272
ARDS
hypoxia
V/Q mismatch
decreased surfactant due to damaged type 2 pneumocytes-decreased compliance, stiffening, bad ventilation-chronic respiratory failure-leads to fibrin deposition
Fibrosis-permanent alveolar damage-leads to chronic hypoxia
273
Gout
elevated uric acid levels-hyperuricemia
overproduction of purines
augmented break down of nucleic acids die to increased cell turnover
thiazides interfere with uric acid excretion
274
Gout attack
monosodium urate crystals precipitate in the joint and initiate an inflammatory response
275
HDL
HDL cholesterol scavenges and removes LDL -- or "bad" -- cholesterol.
HDL reduces, reuses, and recycles LDL cholesterol by transporting it to the liver where it can be reprocessed.
HDL cholesterol acts as a maintenance crew for the inner walls of blood vessels (endothelium). Damage to the endothelium is the first step in the process of atherosclerosis, which causes heart attacks and strokes. HDL chemically scrubs the endothelium clean and keeps it healthy.
What Are Good Levels for the HDL Cholesterol?
A cholesterol test or lipid panel tells the level of HDL cholesterol. What do the numbers mean?
HDL cholesterol levels greater than 60 milligrams per deciliter (mg/dL) are high. That's good.
HDL cholesterol levels less than 40 mg/dL are low. That's bad.
In general, people with high HDL are at lower risk for heart disease. People with low HDL are at higher risk.
What Can I Do if my HDL Cholesterol Level Is Low?
276
Drugs for hypertension
β-Adrenergic blockers work to decrease the heart rate and cardiac output. Diuretics lower blood pressure by decreasing vascular volume, whereas angiotensin-converting enzyme (ACE) inhibitors work to reduce vasoconstriction. Calcium channel blockers reduce blood pressure by a reduction of vascular smooth muscle.
