patho final Flashcards
1
Q
MCV normal finding
A
80-95 - mean corpuscular volume
2
Q
MCH normal finding
A
27-31 - mean corpuscular hemoglobin
3
Q
MCHC normal finding
A
32-36 - mean corpuscular hemoglobin concentration
4
Q
RDW normal finding
A
11-14.5% - red blood cell distribution width
5
Q
MCV
A
average size of single RBC
6
Q
MCH
A
average weight of hemoglobin
7
Q
MCHC
A
average % of hgb within a RBC - can be hypochromic or normochromic
8
Q
RDW
A
variation of size among RBC
9
Q
microcytic normochromic anemia is also called
A
megaloblastic
10
Q
microcytic normochromic anemia labs
A
increased MCV and MCH, normal MCHC, and increased RDW
11
Q
how do you get microcytic normochromic anemia
A
B12 or folate deficiency
12
Q
eryptosis
A
premature death of RBC seen in microcytic normochromic anemia
13
Q
pernicious anemia due to
A
B12 deficiency
14
Q
pernicious anemia labs
A
increased MCV, increased MCH, and increased RDW
15
Q
decreased RBC =
A
decreased blood volume (increased plasma volume)
16
Q
decrease in RBC causes fluid to shift from
A
interstitial space to vascular space because of increased capillary oncotic pressure. this causes the blood to have a decreased viscosity
17
Q
SV and HR with decreased RBC
A
increased SV and HR
18
Q
end product of anemia
A
hypoxemia
19
Q
overall anemia is caused by
A
altered production, blood loss, and increased destruction
20
Q
cytic refers to
A
size
21
Q
chromic refers to
A
HGB
22
Q
absence of intrinsic factor causes
A
B12 deficiency - need intrinsic factor to absorb B12
23
Q
absence of intrinsic factor can be from
A
congenital, chronic gastritis, or gastric bypass
24
Q
B12 deficiency anemia involves and destroys the
A
nervous system through myelin degeneration, paresthesias, gait disturbances, spasticity
25
treatment for pernicious anemia
replace b12
26
b12 can be administered through and will start to work in
subcut injections and needs to be continued throughout life. will correct deficiency in 5-6 weeks
27
if pernicious anemia is not treated
will cause death by HF
28
where is folic acid absorbed from
small intestine and stored in the liver
29
how much folic acid do you need per day
200 mg/day
30
who usually has folic acid deficiency
alcoholics or people with crohn's
31
manifestations of folic acid anemia
cheilosis stomatitis and diarrhea with malabsorption
32
cheilosis stomatitis
inflammation of mouth and lips with crusty bits in corner of mouth
33
folic acid administration can correct deficiency within
1-2 weeks
34
Iron supplement can correct deficiency within
1-2 weeks
35
iron deficiency anemia caused by
chronic blood loss because body isn't able to recycle lost iron
36
what type of pts can have chronic blood loss
pt with ulcers, Ulcerative colitis, cirrhosis, hemorrhoids, esophageal varies
37
iron deficiency anemia s/s
activity intolerance, difficulty swallowing, geriatric confusion/memory loss
38
why do iron deficiency anemia pts have a hard time swallowing
inflamed cells over esophagus which can lead to cancer of the esophagus
39
normocytic-normochromic anemias
normal size and normal hgb but deficient in number - can be aplastic and hemolytic
40
things that cause aplastic anemia
stem cell deficiency, drug reaction, autoimmune, chronic kidney disease
41
what can aplastic cause
SOB and tachycardia and is associated with thrombocytopenia
42
hemolytic anemia
premature destruction of RBC and is hereditary or acquired
43
things that cause hemolytic anemia
G6PD deficiency, sickle cell, blood transfusion reaction, infection, DIC, prosthetic cardiac valves
44
administering blood products helps to
improve tissue oxygenation, increase oncotic pressure, and act as a plasma expander
45
assess before blood product admin
2 RN check, check history of blood products, volume status, and consent
46
what to watch for when administering blood products
immune response and fluid volume overload
47
administer blood product with _________ only
NS
48
PRBCs
packed red blood cells given if hemoglobin less than 7
49
leukocytosis
too many white blood cells - have a physiologic stressor
50
leukopenia
not enough white blood cells because of radiation, autoimmune, or bone marrow depression
51
leukopenia puts you at risk for
infection
52
neutropenia defined as
less than 1000 and becomes life threatening below 500
53
too many eosinophils
allergen
54
too many basophils
inflammation
55
lactic acid occurs during
inflammation - anerobic metabolism byproduct
56
procalcitonin shows for
bacterial infection
57
thrombocytopenia defined as
platelet count below 150,000
58
bleeding with minor trauma platelet count
50,000
59
spontaneous bleeding platelet count
20,000-15,000
60
severe bleeding platelet count
less than 10,000
61
thrombocytopenia can occur from
rare congenital disorders that cause decreased production, nutritional deficiencies, HIV, cancer, drugs, or increased platelet consumption
62
heparin induced thrombocytopenia
immune mediated heparin reaction - IgG antibodies activate thrombin/platelets and put bodying prothrombin state in which platelets group together
63
first indicator of heparin induced thrombocytopenia
50% reduction of platelet count
64
things that can happen during heparin induced thrombocytopenia
DVT, PE, STEMI, ischemia from clots
65
treatment of heparin induced thrombocytopenia
stop all heparin products and start a alternative anticoagulants. test for anti-hep antibody
66
disseminated intravascular coagulation
widespread activation of coagulation - consumption of platelets, clots black vessels and cut off blood flow to organs, and bleeding occurs because clotting factors are all in the clots
67
severity of disseminated intravascular coagulation depends on
intensity of what is causing it
68
causes of disseminated intravascular coagulation
sepsis, solid tumors, pregnancy complications, hemolytic blood transfusion, trauma
69
neoplasm
tumor can be benign to malignant
70
carcinoma
epithelial (skin,GI)
71
adenocarcinoma
cancer of gland or duct
72
sarcoma
cancer of connective, muscle, bone
73
lymphoma
solid tumor on lymphatic tissue
74
leukemia
hematologic (circulating) not a tumor
75
BRCA gene
breast cancer risk
76
PSA gene
prostate cancer risk
77
anaplasia
loss of cellular differentiation
78
pleomorphic
variability of size and shape
79
benign cells are
same size and shape
80
benign tumors
well defined capsule, not invasive, slow growth, low mitotic index
81
malignant tumor
rapid growth, high mitotic index, not encapsulated, invasive
82
paraneoplastic syndrome
cluster of symptoms triggered by a tumor and is usually the first sign of malignancy
83
s/s of paraneoplastic syndrome
anorexia, weight loss, fatigue, fever, cachexia
84
cachexia
weakness and wasting of the body due to severe chronic illness
85
pheochromocytomas
tumor inside the medulla of adrenal gland that secretes sympathetic hormones
86
what other syndromes can be seen with paraneoplastic syndrome
bushings syndrome, pheochromocytomas, DIC, syndrome of inappropriate antidiuretic hormone secretion (SIADH), hypoglycemia
87
chemo is more effective on
rapidly growing cancer cells
88
chemo can cause what dose limiting effects
organ function decline, extravasation, N/V/D (dependent on severity), myelosuppression (dependent on severity)
89
myelosuppression
bone marrow suppression which causes anemia, thrombocytopenia, and leukopenia
90
nadir
10-28 days after chemo WBC will reach a low and put pt at risk for infection
91
normal neutrophil count
55-70%
92
critical WBC count
2.5 or under
93
considerations for pt with low immune system
reverse isolation, limit visitation, hand washing, oral care, food contamination
94
what cause shock
not enough O2 and glucose, impaired cellular metabolism, and inadequate perfusion
95
shock responses
inflammatory and stress response
96
progression of shock causes
multiple organ dysfunction syndrome (MODS) and
97
without treatment shock causes
overwhelms the bodys compensatory mechanisms through positive feedback loops and causes a downward spiral
98
describe what impaired oxygen delivery causes during shock
without O2 the cell shifts to anaerobic metabolism which causes a depletion of ATP and a dysfunction of Na/K pump. Na/K pump dysfunction causes increased intracellular Na/H2O which causes cellular edema and disruption of cell membrane, which causes the release of destructive lysosomes. lysosomes leak into tissues and cause breakdown, inflammation, and activation of clotting cascade which further impairs O2 use and causes a continuous positive feedback loop
99
increased lactic acid levels in shock causes
decrease in PH (an acidic environment) which causes decreased cell function, repair, and division
100
complications of shock
clotting cascade and inflammation - vasodilation, increased vascular permeability, and infiltration of leukocytes. both these further impair O2 use
101
complications of inflammatory response during shock
DIC, ARDS, and acute tubular necrosis
102
shock initially is a ____renal problem but as if progresses
shock initially is a prerenal problem but as if progresses causes tubules to become necrotic and turns into an intrarenal problem
103
describe what impaired glucose delivery causes during shock and why it happens
compensatory mechanisms during shock cause impaired glucose uptake, and because the body is under stress it has high cortisol, T3, T4, and catecholamines which cause insulin resistance (high glucose levels), increased SVR and HR. cells then shift to gluconeogenesis to generate fuel for the high metabolic state. because proteins are being used in gluconeogenesis they are no longer available to maintain cellular structure, function or repair. As these proteins are being broken down the byproduct is ammonia and urea and with less serum protein there is a shift of fluid which causes decreased osmotic pressure and edema. The end product is a buildup of toxins (metabolic waste products) which further decrease cell function, disrupt the membrane and allow lysosomes to be released. shock then becomes irreversible
104
treatment for nonspecific shock
discover and correct cause, expand intravascular volume, counteract vasodilation, supplemental O2, glucose control
105
if there is inadequate volume during shock what med will not work
vasopressors
106
MAP equation
(2 x diastolic + systolic) / 3
107
MAP should be
60 or 65 for adequate tissue perfusion
108
causes of hypovolemic shock
loss of whole blood, loss of plasma through burns or 3rd spacing, or loss of volume through diaphoresis, diuresis, diarrhea, or emesis
109
hypovolemic shock begins to develop when intravascular volume has decreased by
15%
110
initially hypovolemic shock is compensated by
increased HR and SVR
111
s/sx of hypovolemic shock
thready pulse, poor skin turgor, and oliguria
112
treatment for hypovolemic shock
administer fluid (fill up the tank first)
113
treatment for hypovolemic shock
administer fluid (fill up the tank first)
114
alpha 1 receptor
sympathetic response - vasoconstriction, decreased gastric motility, glycogenolysis (increased glucose)
115
alpha 2 receptor
blocks sympathetic activity
116
beta 1 receptor
positive inotropic, chronotropic, and dromotropic forces and renin
117
beta 2 receptor
dilation of bronchioles and glycogenolysis (increasing glucose)
118
inotropic
force
119
chronotropic
HR
120
dromotropic
electrical
121
cardiogenic shock causes
left CHF, MI, dysrhythmias, pericarditis, PE, tamponade, and drugs
122
s/sx of cardiogenic shock
dyspnea, ALOC, dusky skin, hypotension, oliguria, low motility of GI
123
cardiogenic shock definition
decreased cardiac output and tissue hypoxia in the presence of adequate intravascular volume
124
decreased CO causes
activation of RAAS and ADH to increased blood volume
catecholamine release to increase SVR
increased SV, preload and after load, and HR
125
increased SV, preload and after load, and HR causes
systemic and pulmonary edema, increased myocardial oxygen demand, decreased ejection fraction and BP, decreased tissue perfusion, impaired cell metabolism, and myocardial dysfunction
126
anaphylactic shock
IgE antibody causes degranulation of mast cells (histamine release). This provokes an extensive immune and inflammatory response, including vasodilation (decreased SVR), increased vascular permeability (causes hypovolemia and oliguria), and constriction of extravascular smooth muscle. This causes bronchoconstriction and GI cramps which can cause diarrhea
127
CO during anaphylactic shock
normal to high
128
treatment of anaphylactic shock
histamine blockers, steroids, epi, inhaled beta 2 agonist
129
septic shock
bacteria enters into the bloodstream and release toxins which causes an immune response. macrophages come in to fight and TNF and nitric oxide are released. This cause extreme vasodilation, hypo perfusion, and tachycardia. when body becomes overwhelmed systemic inflammatory response syndrome (SIRS) occurs and leads to wide spread tissue hypoxia and necrosis which leads to shock and MODS
130
septic shock treatment
30 mL/kg crystalloids
131
neurogenic shock caused by
parasympathetic overstimulation and sympathetic under stimulation which can occur from spinal cord injury
132
what happens during neurogenic shock
massive vasodilation, decreased vascular tone, decreased SVR, Bradycardia which causes inadequate cardiac output.
133
neurogenic shock treatment
vasopressors
134
rescue drug for methotrexate
leucovorin
135
luecovorin does what
converts to active B9 and preserves normal cells but still allows cancer cells to be killed
136
methotrexate can be administered through
intrathecal admin - administration for drugs via an injection into the spinal canal
137
acute pain is a response from
the sympathetic nervous system
138
chronic pain
pain without a sympathetic response
139
endocannabinoids
phospholipids - modulate pain, sleep, immune function, appetite, and stress response
140
somatic pain
msk pain give NSAIDs
141
visceral
organ pain give opioids
142
number one cause of acute kidney injury
sepsis because of decrease percussion to the kidney
143
kidney labs during acute kidney injury
increased creatinine, increased BUN, decrease GFR
144
signs of acute kidney injury
hyperkalemia, hypermagnesemia, hyperphosphatemia, metabolic acidosis
145
normal BUN level
8-20
146
normal creatinine
0.7-1.4
147
how do you treat prerenal acute renal injury
identify cause and treat the cause and increase BP
148
what happens to GFR, renin, ADH, and NA/h2o during prerenal acute renal injury
decrease GFR and increased renin and ADH. Na and H2O retention
149
harmful AE from morphine
hypotension
150
what electrolyte can cause cardiac arrest if you give it too fast
potassium
151
wrong concentration of what electrolyte can put pt into acute exacerbation of heart failure
sodium
152
DIC
disseminated intravascular coagulation - is a condition in which blood clots form throughout the body, blocking small blood vessels
153
intrarenal acute kidney injury treatment
antibiotic to get rid of infection
154
#1 body system effected by altered sodium level
brain
155
hypokalemia symptoms
irregular pulse and dysrythmias with flattened t and u waves, GI upset, and myalgias to paralysis with respiratory failure
156
hyperkalemia
peaked Ts with widening QRS, myalgias, paralysis, GI upset
157
hyperkalemia treatment
sodium polystyrene sulfonate, calcium gluconate, IV insulin/dextrose, hemodialysis
158
blood in urine =
renal stones
159
top causes of chronic kidney disease
DM- uncontrolled hyperglycemia - causes glucose to stick to artery wall which cause damage to artery supplying blood to kidney
HTN (systemic), glomerulonephritis, lupus, chronic UTI
160
treatment of chronic kidney disease
identification, protection of remaining glomerular function, correct F&E imbalance supplementation, protein restriction, dialysis, and possible renal transplant
161
what medications would you give to chronic kidney disease pt
Ace inhibitors/ARBs, glycemic control, antilipemics, make if patient is on nephrotoxic drugs that the benefit of giving the drug outweighs the risk, and supplementation with Ca, vitamin D, and iron
162
osteoarthritis
degenerative, low grade inflammatory joint disease
163
what happens to joints during osteoarthritis
erosion of cartilage, thickening and inflammation of synovial capsule, osteophytosis, and pain with limited range of motion
164
when cartilage gets broken up the fragments are taken up by the cartilage cells and digested by
the cell's own lysosomal enzymes
165
what 2 things are thought to play a major role in cartilage degradation in osteoarthritis pt
proinflammatory cytokines - interleukin 1 and tumor necrosis factor
166
gout
syndrome caused by either overproduction or under-excretion of uric acid and is characterized by inflammation and pain in the joints
167
osteoporosis
silent progressive bone loss in which pt has more bone resorption and new bone formation
168
postmenopausal induced osteoporosis
from estrogen deficiency which causes and abundance of RANKL and decrease influence of OPG, and more bone destroyers than bone formers
169
what does OPG do
stops bone resorption
170
where exactly in the kidney does blood filtration take place
at the glomerulus
171
what do juxtaglomerular cells do
they regulate renal blood flow and systemic blood pressure by secreting renin
172
2 natural (hormonal) antagonists to the RAA system
urodilatin and BNP
173
RANKL
The interaction of RANK with its ligand (RANKL) has been identified as the final common pathway through which bone resorption is regulated
174
lactic acid is used as a marker for the
severity of sepsis
175
GFR of kidney failure
below 15
176
GFR of kidney disease
15-60
177
what is urea
waste product produced from liver breaking down protein
178
How can myoglobin cause infrarenal injury?
excess myoglobin may thus cause renal tubular obstruction, direct nephrotoxicity (ischemia and tubular injury), intrarenal vasoconstriction
179
why does chronic kidney disease cause bone pain
- Kidneys activate vitamin D – helps absorb Ca in CKD kidney not activating vitamin D so low calcium and High phosphate levels cause even lower calcium levels because calcium binds to phosphate
- Hyperparathyroidism
- Parathyroid gland secrete parathyroid hormone when calcium levels are low
- Parathyroid hormone indirectly influences osteoclast by stimulating the bones to release calcium into the blood = decreased bone health and possible bone pain
180
what does chronic kidney disease do to CV and pulmonary system
causes pulmonary edema, HTN, HF, edema
181
why does chronic kidney disease cause Anemia, epistaxis (nose bleed), bruising
because of the reduced erythropoietin secretion and toxins alter platelet function. patient can look pale
182
why does chronic kidney disease cause N/V and anorexia
retention of metabolic acids and waste products
183
what type of skin problems can you see on a CKD patient
pruritic excoriations, frost, sallow pigmentation, discolored nails
184
CKD and muscles
myopathy (muscle weakness) – due to decrease amount of protein
185
why can CKD pt have hypothyroidism
Uremia delays the response of thyroid stimulating hormone receptors and Ts levels are often low
186
insulin resistance in chronic kidney pt
Related to proinflammatory cytokines and alterations in adipokines (causes high leptin and low adiponectin)
187
what happens to your immune system with CKD
Immune system is suppressed due to uremia (high level of urea in blood)
188
what structure actually produces the urine
nephrons
189
what shows up in urine during CKD
protein and blood
190
why do CKD pt get metabolic acidosis
because there is a diminished ability to excrete H+ and generate bicarb which leads to acidosis
191
EKG during hypokalemia
long QU interval and prominent U waves
192
EKG during hyperkalemia
peaked T waves
193
EKG during hypocalcemia
QT prolongation
194
EKG during hypercalcemia
shortening of the ST segment
195
steps to late stage of CKD
1. HTN in arteries going to the kidney which causes release of renin which causes more HTN and over time will cause vessel thickening and narrowing which will lead to glomerulosclerosis.
2. sclerosis causes ischemic injury and nephron loss
3. nephrons are compensating for other lost nephrons so there is glomerular hyperfiltration that is tolerated during early stages, but not in late
4. hyperfiltration causes more sclerosis from the pressure
5. more loss if nephrons
6. nephrons can not compensate any more and you have a decrease in GFR
196
what does gastrin do?
stimulates gastric glands to secrete HCl, pepsinogen, and histamine
197
what does acetylcholine do to the stomach
stimulates the release of pepsinogen and acid secretion
198
what do prostaglandins do
regulate perfusion to stomach, regulates mucus to release bicarb, and controls acid amount secreted by parietal cells
199
what do the parietal cells do
secrete HCl and intrinsic factor
200
what happens if your stomach is empty but your stressed so your stomach is still secreting gastrin and histamine
gastrin stimulates stomach to release pepsinogen which is turned into pepsin and can cause ulcers
201
what is intrinsic factor needed for
absorption of B12
202
what happens in your stomach when you eat food
Food stimulates gastrin
Gastrin stimulates parietal cells to release HCl, intrinsic factor, histamine, and stimulates chief cells to release pepsinogen
Histamine stimulates more acid secretion
Pepsinogen - breakdown protein and turn into pepsin
Intrinsic factor needed for B12 absorption
203
hematochezia vs melena
both are a type of GI bleed. hematochezia is bright red filled with blood clots, not digested blood- shows problem in lower GI. Melena is coffee ground - dark, digested blood from upper GI
204
what meds can people take for gastritis
PPIs or H2 blockers
205
how duodenal ulcers form
usually from H. Pylori which activates T and B lymphocytes and neutrophil infiltration and release of inflammatory cytokines which damage the gastric epithelium. they can also occur form acid and pepsin not deactivating when entering the duodenum
206
gastric ulcer caused by
a break in the mucosa that allow hydrogen ions to diffuse through the mucosa which causes damage and release of histamine
207
the release of histamine during gastric ulcers cause
increase blood flow from vasodilation and increased permeability. this all causes loss of plasma proteins and damaged vessels which causes bleeding
208
H2 receptor antagonist do what
decrease acetylcholine and gastrin. increases the ph and reduces the H+ secretion from the parietal cells
209
nursing consideration for Pepcid
H2 receptor antagonist - dilute with 5-10 ml of NS and push over 2 minutes or can cause hypotension
210
liver metabolizes
glucose and stores it as glycogen and converts glycogen to glucose
211
what happens with glucose in liver disease patients
they can get hepatic diabetes from chronic high blood glucose levels
212
what is the byproduct of protein metabolism
ammonia
213
what does the liver do with ammonia
converts it to urea so if the liver is not functioning properly a build up of ammonia can occur
214
liver stores
vitamins B12, A, C, E, D, and K
215
vitamin D does what
helps absorb calcium
216
vitamin K does what
helps the clotting process
217
liver helps with the production of
blood plasma proteins
218
portal hypertension
abnormally high blood pressure in the portal venous system caused by resistance to blood flow
219
intrahepatic causes of portal hypertension
inflammation, fibrosis, and vascular remodeling that occur from cirrhosis or hepatitis
220
post hepatic causes of portal hypertension
impaired pumping of the heart or obstruction from Right HF or thrombus
221
consequences of long term portal hypertension
varices, splenomegaly, hepatopulmonary syndrome, portopulmonary hypertension
222
most common symptom of splenomegaly
thrombocytopenia (low platelets)
223
hepatopulmonary syndrome
shunting occurs because pressure causes new vascular pathway and this new pathway does not pass the alveoli to obtain new oxygen. when the blood that went through the shunt meets up with the oxygenated blood that went through normal pathway the overall blood oxygen level is lower than if there wasnt a shunt. This causes hypoxemia
224
factor that contribute to the development of ascites
decreased synthesis of albumin by the liver, portal hypertension, and splanchnic arterial vasodilation
225
what does increased nitric oxide do
can decrease effective circulating blood volume which activates RAAS (aldosterone) and antidiuretic hormone, which promotes renal sodium and water retention and overall accelerates portal hypertension and ascites
226
hepatic encephalopathy
complex neurologic syndrome where toxins effect neurotransmission because the liver is not able to convert ammonia to urea in its toxic state
227
jaundice results from either
obstructive or hemolytic cause
228
extrahepatic causes of jaundice
liver still working but bilirubin accumulation because gallstone blockage of bile flow- considered conjugated
229
conjugated
hepatocytes functioning so something else is causing the problem
230
unconjugated
hepatocytes not functioning so they are the cause of the problem
231
liver labs will be normal in what type of jaundice
extrahepatic jaundice
232
fibrosis in the liver of cirrhosis patients is a consequence of
infiltration of leukocytes and release of inflammatory mediators
233
ulcerative colitis is mainly in the compared to crohn's which can be
ulcerative colitis is continuous lesions that occur mainly in the large intestine while Crohn's has skip lesions that can occur anywhere from mouth to anus
234
treatment of ulcerative colitis vs Crohn's
ulcerative colitis is cured with surgery of taking out the entire colon. Crohn's is not curable and is managed with surgery
235
excessive cortical =
Cushing syndrome
236
excessive ACTH
Cushing disease
237
what does cortisol do to our bodies
increases blood pressure and cardiac output, increases blood levels of amino acids, and decreases luteinizing hormones, estradiol, and testosterone
238
cause of cushing disease
caused by a tumor either in pituitary or adrenal
239
cause of Cushing syndrome
excessive/long term steroid use or can happen in people with long term high levels of stress
240
stress hormones do what to our BP and glucose
they are vasoconstrictors so will increase BP and increase blood glucose levels
241
negative feedback loop for adrenal gland regulation
it begins when low circulating corticosteroid hormones are noticed by the hypothalamus or when stress is present. hypothalamus responds by releasing corticotropin releasing hormone which causes anterior pituitary to release adrenocorticotropic hormone (ACTH), this stimulates adrenal cortex to release cortisol. once the threshold of corticosteroids is reached the hypothalamus inhibits the release of corticotropin releasing hormone (CRH).
242
glucocorticoid function
carbohydrate metabolism, protein breakdown in the muscle tissue, immune/inflammatory suppression, inhibition of bone formation, nerve function depression, and increase effect of catecholamine response
243
mineralocorticoid function
sodium retention, potassium/H+ loss, BP control, increase cardiac contraction, increase systemic vascular resistance, and decrease fibrolysis
244
calcitonin is secreted by the thyroid when
circulating calcium levels are too high
245
negative feedback loop of the thyroid gland
when circulating thyroid hormones are low the hypothalamus releases thyroid releasing hormone (TRH), this stimulates the anterior pituitary gland to secrete thyroid stimulating hormone (TSH), this stimulates the thyroid to release T3 and T4, T3 and T4 bind to proteins but once the unbound amount of circulating T3 and T4 levels are sufficient the hypothalamus halts the release of thyroid releasing hormone
246
function of T3 and T4
regulates protein, fat, and carbohydrate catabolism, metabolic rate, and body heat production. maintains growth hormone secretion, cardiac rate, force, output, secretion of GI tract, and calcium mobilization. affects RR, RBC production, and CNS development
247
what happens with weight during cushing syndrome
weight gain with a redistribution of fat
248
what happens with glucose in Cushing syndrome
glucose intolerance occurs because of cortisol induces insulin resistance and increased gluconeogenesis
249
what does cushing's syndrome do to the integumentary system
weakens the integumentary system due to loss in collagen which causes the skin to be thin and causes capillaries to become weaker and seen through the skin. this amounts for striae and bruising
250
what does protein wasting cause and what syndrome causes it
protein wasting occurs in cushing syndrome from the catabolic effect of cortisol. it causes muscle loss, bone wasting, and is the cause of the weakened integumentary system too
251
bone wasting causes
increase fracture risk, increase risk of osteoporosis, hypercalciuria, and risk of stones
252
the elevated levels in cushing syndrome will cause
vasoconstriction, HTN, increase risk of infection, mental status change in up to 50% of pt, and mineralocorticoid effects such as water and sodium retention, and increased adrenal androgen
253
treatment for cushing syndrome
managing hyperglycemia, HTN, hypokalemia, and metabolic alkalosis. possible stress dosing. radiation, surgery, gradual cessation of steroids, help with the patients with disturbed body image
254
hyposecretion of cortisones and aldosterone
Addison disease
255
lab levels during Addisons disease
low cortisol, low aldosterone, high ACTH because of the loss in negative feedback. low sodium, low glucose, fluid volume deficit, increased potassium, increased BUN, and high WBC because autoimmune
256
signs and symptoms of Addison disease
weight loss, fatigue, N/V/D, skin changes, infection
257
treatment of Addison disease
lifetime fludrocortisone and glucocorticoid, a minimum of 3400 mg of sodium per day, and low stress
258
adrenal crisis can be caused by
Addison disease or stopping exogenous steroids too fast
259
what occurs during an adrenal crisis
hypotension, vascular collapse, hypovolemic shock
260
priority treatment for Adrenal crisis
administer cortisol
261
hyperthyroid labs
low TSH and high T3 and T4
262
hypothyroid labs
high TSH and low T3 and T4
263
thyrotoxic storm labs
normal TSH, super high T3 and T4 because brain hasn't turned TSH off yet - this is an acute problem
264
graves disease
primary hyperthyroidism due to autoimmune disease
265
signs of graves disease
exophthalmos and pretrial myx-edema
266
hyperthyroidism treatment
antithyroid drugs, surgery - removal of the thyroid, radioactive iodine therapy, beta blockers, and symptom relief
267
thyrotoxic crisis treatment
anti thyroid drug, beta blockers for control of cardiovascular symptoms, steroids
268
manifestation of hypothyroidism
low metabolic rate, cold intolerance, lethargy, bradycardia, goiter
269
secondary hypothyroidism causes
traumatic brain injury, Subarachnoid hemorrhage, or pituitary tumors or infarction
270
myxedema coma causes
decrease LOC, hypotension, hypoglycemia, hypothermia, hypoventilation which causes hypoxia and can lead to lactic acidosis
271
folliculitis
infection of the hair follicle that is caused by bacterial, fungal, and viral infection but S. aureus is the predominant culprit
272
furuncles
"boils" - folliculitis that is spread to dermal tissue
273
carbuncle
collection of infected hair follicles that extends into the subcutaneous tissue
274
characteristics of carbuncle
systemic complications - fever, chills, weakness
| abscess may develop
275
Cellulitis
infection of the dermis and subcutaneous tissue usually caused by S. aureus
276
what is needed for cellulitis
systemic antibiotic
277
treatment for CRE
only 2 antibiotics are able to treat it but one of them had a "all-cause mortality" BBW
278
When is a mineralocorticoid released by the adrenal cortex
Mineralocorticoid is released by the adrenal cortex in response to angiotensin II, but overall is stimulated by low sodium and water depletion, increased potassium levels, and diminished blood volume.
279
You notice your patient is exhibiting itching, throat swelling and a fast irregular pulse. Which three medications would you anticipate administering swiftly
Epinephrine, diphenhydramine, and famotidine
280
Name one response the GI system has to a release of serotonin
Serotonin causes vasodilation in the gut.
281
Identify the ABG abnormality associated with vomiting/ diarrhea, respectively.
Vomiting is associated with metabolic alkalosis and Diarrhea is associated with metabolic acidosis.
282
List the 7 (yes, 7) main functions of the liver.
1. Formation and secretion of bile
2. Metabolism of bilirubin
3. Stores blood, syntheses of clothing factors, and bile production
4. metabolism of fats and nutrients and releases and absorbs glucose and stores glycogen
5. metabolic detoxification
6. storage of vitamins and minerals
7. synthesis of thrombopoietin
283
how does the stomach lining survive through the acidic environment
prostaglandins are simulated to secrete mucus that creates a barrier to protect the stomach
284
neurotransmitter released when food enter into the duodenum
serotonin which causes and increase in GI mobility and vasodilation in gut
285
minimum inhibitory concentration
lowest amount of antibiotics needed to kill a bacteria includes how long the patient is on and the concentration
286
treatment for inflammatory bowel disease
corticosteroids to keep inflammation down now, biologics, immunomodulators- keep inflammation down in future, antibiotics, and treat symptoms -anti-diarrheal and nutritional deficiencies (anemia)
287
bacteriostatic
inhibit growth of bacteria
288
general anemia patho
decreased RBC which causes fluid to move into vascular space and blood gets thiner which causes blood to move faster and more turbulent through the vessels. This causes tress on the heart and increases stroke volume and heart rate. end result can be high output heart failure. blood will flow to vital organs and there will be a decreased blood flow to the kidney which will cause activation of RAAS and even more fluid build up.
289
general signs of anemia
lethargy, pale/jaundice, abd pain/N/V due to decreased blood to GI, SOB, low fever, impaired healing, tachycardia, HF, difficulty walking, paresthesias of hands and feet because of myelin degeneration in B12 deficient anemia
290
iron supplements
Ferrous sulfate, iron dextran, and iron sucrose
291
ferrous sulfate
oral - no dairy or antacids. OJ increases absorption. sit upright for 30 min
292
Iron dextran
IV - need test dose before, watch for anaphylaxis and hypotension
293
iron sucrose
IV - don't need test dose before. watch for hypotension
294
macrocytic normochromic anemias
pernicious and folic acid deficient
295
microcytic hypochromic anemia
iron deficiency
296
normocytic normochromic anemias
aplastic and hemolytic
297
if pt is on furosemide what else should they be on
K supplement
298
opioid reversal
naloxone
299
MG sulfate
IV - can cause tornadoes de pointes (ribbon shape on EKG)
300
MG oxide
supplement (oral)
301
MG citrate
laxative
302
phenazzopyridine (Pyridium)
for pain caused by UTI
303
cyclosporin
med given for organ rejection prevention
304
antibiotics given for IBS
ciprofloxacin or flagyl
305
pharmacological treatment for IBS
corticosteroids, biologics (anti-ca, anti-TNF), immunomodulators, antibiotics, and antidiarrheals
306
antidiarrheals
non-opiate: belladonna alkaloid (donnatal elixir)
| opiate: lomotil and Imodium
307
psyllium (Metamucil)
bulk forming laxative
308
glucocorticoids
hydrocortisone, solu-medrol, prednisone, dexamethasone
309
mineralcorticoid
fludrocortisone for Addisons disease
310
antithyroid drugs
methimazole (tapazole) and PTU
311
epinephrine does what
vasoconstrictor and bronchodilator - nonselective adrenergic agonist
312
Bactrim
sulfonamide for UTI but has hypoglycemic effect with sulfonylureas, encephalopathy effect with phenytoin, and nephrotoxic with cyclosporin
313
PCN G IM
uncomplicated syphilis
314
pipercillin/tazzobactam (Zosyn)
beta lactase inhibitor for H-A infection, PNA, or sepsis
315
cefazolin (ancef)
1st generation cephalosporin for surgical prophylaxis - has most gram positive coverage
316
cefepime (maxipime)
4th generation cephalosporin for complicated UTI, PNA and skin infection
317
ceftaroline (Teflaro)
5th generation cephalosporin for MRSA and PNA
318
meropenem (merrem)
carbapenem antibiotic - for MRSA PNA sepsis UTI
319
ertapenem (invanz)
carbapenem antibiotic - for MRSA PNA sepsis UTI
320
erythromycin
macrolide antibiotic - for eye/skin infection, chlamydia, gonorrhea - causes increased GI motility and has more AE than azithromycin
321
tobramycin
aminoglycocide antibiotic - for resistant gran negative bacteria but can be oto/nephro/neuro toxic
322
what is different in septic shock metabolism
plasma protein breakdown includes the metabolism of immunoglobulins which impairs the immune system function when it is most needed.
323
septic anaerobic metabolism
protein metabolism releases alanine which converts into pyretic acid which is sepsis is converted into lactic acid and worsens metabolic acidosis and glucose metabolism
324
Identify 2 key functions of the hematologic system.
Hematologic system provides oxygen and nutrients to tissues and help defend against foreign invaders. They also help us repair from traumatic injury.
325
Identify 2 inorganic or organic molecules that albumin can transport.
Albumin can transfer drugs and other blood components. These blood components include vitamins, hormones, and lipids.
326
Where are the sites of active red bone marrow? (provide two specific bones)
Sites are in flat bones such as the skull and vertebrae.
327
What is the normal hematocrit for both men and women
48% of blood volume in men
| 42% of blood volume in women
328
Why do patients with sickle cell anemia have a difficult time maintaining oxygenation?
Patients with sickle cell anemia have a crescent shaped red blood cell. This makes it difficult for the red blood cells to maintain a good flow, which overall decreases the ability to maintain oxygenation. These patients need a steady flow of oxygen.
329
Name three stimuli for accelerated erythropoiesis.
Stimuli that accelerate erythropoiesis are decline in arterial oxygen levels and tissue hypoxia, high altitude, anemia, and pulmonary disease.
330
Eosinophils release which 3 enzymes that help control inflammatory processes?
Eosinophils release prostaglandins, leukotrienes, and histamine.
331
Lymphocytes are the primary cells in which type of immunity?
Lymphocytes are the primary cells in adaptive immunity.
332
Patients are usually asymptomatic until platelet counts drop below _______ and spontaneous bleeding usually does not occur until platelet counts are below ________.
Patients are usually asymptomatic until platelet counts drop below 100,000 and spontaneous bleeding usually does not occur until platelet counts are below 20,000.
