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Nursing school level 2 > 332 test 2 > Flashcards

332 test 2 Flashcards

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1
Q

what secretion increases when you eat and during stress

A

gastrin secretion

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2
Q

what does gastrin do?

A

stimulates gastric glands to secrete HCl, pepsinogen, and histamine

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3
Q

what stimulates histamine to be released in mucosa of stomach

A

gastrin

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4
Q

what does histamine in the stomach do

A

stimulates acid secretion

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5
Q

what stimulates acetylcholine in the stomach

A

vagus and local nerves in the stomach

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6
Q

what does acetylcholine do to the stomach

A

stimulates the release of pepsinogen and acid secretion

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7
Q

what do prostaglandins do

A

regulate perfusion to stomach, regulates mucus to release bicarb, and controls acid amount secreted by parietal cells

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8
Q

what do the parietal cells do

A

secrete HCl and intrinsic factor

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9
Q

what do chief cells do

A

release pepsinogen to breakdown protein

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10
Q

what happens if your stomach is empty but your stressed so your stomach is still secreting gastrin and histamine

A

gastrin stimulates stomach to release pepsinogen which is turned into pepsin and can cause ulcers

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11
Q

what is intrinsic factor needed for

A

absorption of B12

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12
Q

what happens in your stomach when you eat food

A

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

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13
Q

risk factors to gastritis/peptic ulcer disease

A

alcohol, stress, caffeine, fatty meals, NSAID use, H. Pylori, smoking (vaping)

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14
Q

Gastritis

A

inflammatory erosion in the stomach related to increased HCl

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15
Q

not considered an ulcer until

A

erosive factors that have overcome protective factors get deep enough to hit the bloodstream

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16
Q

is gastritis does not resolve it can turn into

A

chronic gastritis or peptic ulcer disease

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17
Q

signs and symptoms of gastritis

A

epigastric pain, nausea, vomiting, GI bleeding

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18
Q

chronic gastritis can cause

A

pernicious anemia

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19
Q

what is pernicious anemia

A

anemia due to low B12 absorption

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20
Q

hematochezia vs melena

A

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

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21
Q

treatment for gastritis

A

soft bland diet, but if from h. Pylori should take antibiotics

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22
Q

what lab do you want to pay attention to with gastritis

A

H&H

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23
Q

what meds can people take for gastritis

A

PPIs or H2 blockers

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24
Q

what happens to the GI mucosa in peptic ulcer disease

A

the GI mucosa is digested by pepsin

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25
Q

NSAIDs do what

A

block prostaglandin synthesis

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26
Q

Zollinger Ellison syndrome

A

syndrome associated with peptic ulcer disease caused by neuroendocrine gastrin secreting tumor which causes excess secretion of gastric acid

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27
Q

treatment for H. pylori

A

PPI and antibiotic

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28
Q

which type of ulcers occur more often

A

duodenal ulcers

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29
Q

how duodenal ulcers form

A

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

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30
Q

peptic ulcer disease can lead to high risk of

A

gastric cancer

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31
Q

sign and symptoms of duodenal ulcer

A

pain 2-3 hours after eating and in the middle of the night

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32
Q

sign and symptoms or gastric ulcer

A

pain right after eating

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33
Q

gastric ulcer caused by

A

a break in the mucosa that allow hydrogen ions to diffuse through the mucosa which causes damage and release of histamine

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34
Q

the release of histamine during gastric ulcers cause

A

increase blood flow from vasodilation and increased permeability. this all causes loss of plasma proteins and damaged vessels which causes bleeding

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35
Q

secretin does what

A

influences the environment of the duodenum by regulating secretions in the stomach, pancreas, and liver.

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36
Q

what can affect the effectiveness of H2 receptor antagonist

A

smoking

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37
Q

H2 receptor antagonist do what

A

decrease acetylcholine and gastrin. increases the ph and reduces the H+ secretion from the parietal cells

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38
Q

example of H2 receptor antagonist

A

famotidine (Pepcid)

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39
Q

what other drugs should not be given with H2 receptor antagonist

A

drugs that need to be broken down because of the decreased amount of gastric acid so it will mess with the absorption

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40
Q

nursing consideration for Pepcid

A

dilute with 5-10 ml of NS and push over 2 minutes or can cause hypotension

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41
Q

where is the vomiting center

A

in the brain

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42
Q

what causes vomiting sensation

A

neurotransmitter stimulate chemoreceptor trigger zone

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43
Q

should you drink water right after vomiting

A

no inhibit it for 30 minutes after

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44
Q

what drugs can be used as adjust with nausea and vomiting

A

dexamethasone and lorazepam

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45
Q

liver metabolizes

A

glucose and stores it as glycogen and converts glycogen to glucose

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46
Q

what happens with glucose in liver disease patients

A

they can get hepatic diabetes from chronic high blood glucose levels

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47
Q

what is the byproduct of protein metabolism

A

ammonia

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48
Q

what does the liver do with ammonia

A

converts it to urea so if the liver is not functioning properly a build up of ammonia can occur

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49
Q

liver stores

A

vitamins B12, A, C, E, D, and K

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50
Q

vitamin D does what

A

helps absorb calcium

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51
Q

vitamin K does what

A

helps the clotting process

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52
Q

liver helps with the production of

A

blood plasma proteins

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53
Q

portal hypertension

A

abnormally high blood pressure in the portal venous system caused by resistance to blood flow

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54
Q

where does the blood in the hepatic portal vein come from

A

all the organs that play a role in digestion so the stomach, spleen, pancreas, and intestines

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55
Q

intrahepatic causes of portal hypertension

A

inflammation, fibrosis, and vascular remodeling that occur from cirrhosis or hepatitis

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56
Q

post hepatic causes of portal hypertension

A

impaired pumping of the heart or obstruction from Right HF or thrombus

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57
Q

consequences of long term portal hypertension

A

varices, splenomegaly, hepatopulmonary syndrome, portopulmonary hypertension

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58
Q

varices

A

distended veins from obstruction/pressure. blood then is shunted and pushed into other areas including the abdominal wall, stomach and esophagus

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59
Q

why are varies life threatening

A

because the vessels can rupture and lose a lot of blood

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60
Q

splenomegaly

A

enlarged spleen caused by increased pressure in the splenic vein which branches from the portal vein

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61
Q

most common symptom of splenomegaly

A

thrombocytopenia (low platelets)

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62
Q

hepatopulmonary syndrome

A

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

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63
Q

portopulmonary hypertension

A

the pressure buildup in the portal vein causes remodeling and pulmonary vasoconstriction

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64
Q

ascites

A

accumulation of fluid in the peritoneal cavity

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65
Q

most common cause of ascites

A

cirrhosis

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66
Q

factor that contribute to the development of ascites

A

decreased synthesis of albumin by the liver, portal hypertension, and splanchnic arterial vasodilation

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67
Q

what do decreased albumin levels and portal hypertension do to pressure gradient

A

cause capillary hydrostatic pressure to exceed capillary osmotic pressure which pushes water into the peritoneal cavity (ascites)

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68
Q

what is splanchnic arterial vasodilation associated with

A

increased production of nitric oxide by a diseased liver

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69
Q

what does increased nitric oxide do

A

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

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70
Q

goal for ascites

A

palliative care (comfort) this can include paracentesis

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71
Q

what to watch out for during paracentesis

A

taking off too much fluid can cause the patient’s blood pressure to drop dramatically

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72
Q

hepatic encephalopathy

A

complex neurologic syndrome where toxins effect neurotransmission because the liver is not able to convert ammonia to urea in its toxic state

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73
Q

symptoms of hepatic encephalopathy

A

range from lethargy to coma

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74
Q

what can hepatic encephalopathy cause

A

astrocyte swelling from elevated ammonia levels, altered Blood brain barrier, and cerebral edema

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75
Q

treatment for hepatic encephalopathy

A

fluid and electrolyte maintenance, cessation of depressant drugs, protein restriction

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76
Q

jaundice results from either

A

obstructive or hemolytic cause

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77
Q

obstructive cause of jaundice can either be

A

extrahepatic or intrahepatic

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78
Q

extrahepatic causes of jaundice

A

liver still working but bilirubin accumulation because gallstone blockage of bile flow- considered conjugated

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79
Q

conjugated

A

hepatocytes functioning so something else is causing the problem

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80
Q

unconjugated

A

hepatocytes not functioning so they are the cause of the problem

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81
Q

intrahepatic cause of jaundice

A

hepatocyte dysfunction so liver has decreased ability to excrete bilirubin

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82
Q

hemolytic cause of jaundice

A

excesses hemolysis of red blood cells and liver can’t keep up with the amount of RBC that need to be recycled

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83
Q

liver labs will be normal in what type of jaundice

A

extrahepatic jaundice

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84
Q

hepatorenal syndrome

A

functional kidney failure that develops as a complication of advanced liver disease, so the failure of the kidney does not happen because of kidney problems but because extrinsic factors due to liver disease

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85
Q

cause of hepatorenal syndrome

A

hypotension and vasodilation from variceal bleeding due to liver disease or hypotension due to abdominal paracentesis can causes prerenal acute kidney injury - hypoperfusion
portalhypertension - accumulation of blood in kidney
circulatory problems and cardiac impairment: such as right HF which decreases cardiac output

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86
Q

cirrhosis

A

irreversible, inflammatory, and fibrotic liver disease

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87
Q

causes of cirrhosis

A

hepatitis a/b/c, right HF, alcohol, autoimmune/hereditary, and idiopathic (unknown)

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88
Q

structural changes in cirrhosis are caused by

A

injury from viruses/toxicity from alcohol and fibrosis

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89
Q

fibrosis in the liver of cirrhosis patients is a consequence of

A

infiltration of leukocytes and release of inflammatory mediators

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90
Q

nonalcoholic fatty liver disease is associated with

A

obesity, high triglycerides, and DM 2

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91
Q

nonalcoholic fatty liver disease signs and symptoms

A

often asymptomatic for years because it progresses slowly

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92
Q

the most severe forms of nonalcoholic fatty liver disease will progress to

A

cirrhosis and end stage liver disease

93
Q

inflammatory bowel disease includes

A

ulcerative colitis and crohns

94
Q

ulcerative colitis is mainly in the compared to crohn’s which can be

A

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

95
Q

inflammation in ulcerative colitis vs Crohn’s

A

inflammation in ulcerative colitis is in the mucosal layer while Crohn’s involves the entire intestinal wall

96
Q

clinical manifestations in ulcerative colitis vs Crohn’s

A

ulcerative colitis will have prominent diarrhea, bloody stools, and will not have weight loss. Crohn’s will have weight loss due to small intestine malabsorption, may or may not have diarrhea, and blood in stools is less common

97
Q

treatment of ulcerative colitis vs Crohn’s

A

ulcerative colitis is cured with surgery of taking out the entire colon. Crohn’s is not curable and is managed with surgery

98
Q

out of ulcerative colitis vs Crohn’s which can form into abscesses and necrosis and which can form into anal fistulas, obsesses, and obstructions

A

ulcerative colitis can form into abscesses and necrosis and Crohn’s can form into anal fistulas, obsesses, and obstructions

99
Q

chronic inflammatory bowel diseases are diseases of

A

remission and exacerbations

100
Q

chronic inflammatory bowel diseases increase risk for

A

cancer - ulcerative colitis had a higher risk than Crohn’s

101
Q

causes of constipation

A

dehydration, suppression of the urge to go, impaired colonic motor activity, pelvic floor/anal dysfunction, drugs, endocrine disorders, aging, pregnancy, and colorectal cancer

102
Q

what would cause a patient to have pelvic floor/anal dysfunction

A

neurogenic disorders such as paralysis

103
Q

what would cause a patient to have impaired colonic motor activity

A

a low residual diet (low fiber)

104
Q

what drugs cause constipation

A

opioids, calcium or aluminum antacids, anticholinergics, and iron

105
Q

endocrine disorders that can cause constipation

A

hypothyroidism and DM

106
Q

ways to treat constipation

A

dietary, behavior, pharmacological including enemas, and if really ban through surgery

107
Q

excessive cortical =

A

Cushing syndrome

108
Q

excessive ACTH

A

Cushing disease

109
Q

anemia in ulcerative colitis vs Crohn’s

A

ulcerative colitis can have blood loss anemia vs Crohn’s can have macrocytic anemia from low B9 and B12 absorption

110
Q

what does cortisol do to our bodies

A

increases blood pressure and cardiac output, increases blood levels of amino acids, and decreases luteinizing hormones, estradiol, and testosterone

111
Q

cause of cushing disease

A

caused by a tumor either in pituitary or adrenal

112
Q

cause of Cushing syndrome

A

excessive/long term steroid use or can happen in people with long term high levels of stress

113
Q

what are two things that occur in people with hypercortisolism aka cushings syndrome

A

their normal diurnal and circadian secretion patterns pf ACTH and cortisol are lost (disrupts their sleep and wake cycle) and there is no increase in ACTH or cortisol in response to stressors (normally there should be an increase in ACTH and cortisol during stress)

114
Q

hormonal regulation occurs in response to

A

chemical factors, endocrine factors, or control from the nervous system in response to stimuli

115
Q

negative feedback loop of hormones

A

occurs when there is a neural, chemical, or endocrine response to stimulus that decreases the synthesis and secretion of a hormone

116
Q

stress hormones do what to our BP and glucose

A

they are vasoconstrictors so will increase BP and increase blood glucose levels

117
Q

adrenal cortex secretes

A

corticosteroids in response to low circulating cortisol levels, diurnal patterns of wake and sleep, and stress

118
Q

endogenous glucosorticoid =

A

cortisol

119
Q

endogenous mineralocorticoid

A

aldosterone

120
Q

negative feedback loop for adrenal gland regulation

A

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).

121
Q

glucocorticoid function

A

carbohydrate metabolism, protein breakdown in the muscle tissue, immune/inflammatory suppression, inhibition of bone formation, nerve function depression, and increase effect of catecholamine response

122
Q

mineralocorticoid function

A

sodium retention, potassium/H+ loss, BP control, increase cardiac contraction, increase systemic vascular resistance, and decrease fibrolysis

123
Q

how do glucocorticoids promote carbohydrate metabolism

A

by promoting gluconeogenesis in the liver and decreasing glucose uptake thus promoting insulin resistance

124
Q

calcitonin is secreted by the thyroid when

A

circulating calcium levels are too high

125
Q

negative feedback loop of the thyroid gland

A

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

126
Q

what is required for the synthesis of T3 and T4

A

iodine

127
Q

function of T3 and T4

A

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

128
Q

calcitonin function

A

lowers serum calcium levels by opposing bone resorbing effects of parathyroid by inhibiting osteoclast activity, lowers phosphate levels by decreases calcium and phosphate absorption in GI tract

129
Q

what happens with weight during cushing syndrome

A

weight gain with a redistribution of fat

130
Q

what happens with glucose in Cushing syndrome

A

glucose intolerance occurs because of cortisol induces insulin resistance and increased gluconeogenesis

131
Q

what does cortisol induces insulin resistance cause

A

polyuria and glycosuria and 20% of individuals with Cushing syndrome will develop DM

132
Q

what does cushing’s syndrome do to the integumentary system

A

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

133
Q

what does protein wasting cause and what syndrome causes it

A

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

134
Q

bone wasting causes

A

increase fracture risk, increase risk of osteoporosis, hypercalciuria, and risk of stones

135
Q

if you have hypercalciuria then you most likely have

A

hypocalcemia

136
Q

the elevated levels in cushing syndrome will cause

A

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

137
Q

what does increased adrenal androgen do to the body

A

can cause symptoms of virilization

138
Q

virilization

A

taking on the characteristics of men such as increased hair growth…

139
Q

treatment for cushing syndrome

A

managing hyperglycemia, HTN, hypokalemia, and metabolic alkalosis. possible stress dosing. radiation, surgery, gradual cessation of steroids, help with the patients with disturbed body image

140
Q

without treatment for cushing syndrome

A

50% of patients die within 5 years due to infection, HTN, or suicide

141
Q

hyposecretion of cortisones and aldosterone

A

Addison disease

142
Q

Addisons disease is caused by

A

autoimmune mechanism that destroy adrenal cells

143
Q

lab levels during Addisons disease

A

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

144
Q

usually don’t see the signs and symptoms of Addisons until

A

90% of the adrenocortical tissue is destroyed

145
Q

what causes the hypo section or steroids in Addisons disease

A

inadequate stimulation and inadequate synthesis of the steroids

146
Q

signs and symptoms of Addison disease

A

weight loss, fatigue, N/V/D, skin changes, infection

147
Q

treatment of Addison disease

A

lifetime fludrocortisone and glucocorticoid, a minimum of 3400 mg of sodium per day, and low stress

148
Q

adrenal crisis can be caused by

A

Addison disease or stopping exogenous steroids too fast

149
Q

what occurs during an adrenal crisis

A

hypotension, vascular collapse, hypovolemic shock

150
Q

priority treatment for Adrenal crisis

A

administer cortisol

151
Q

hyperthyroid labs

A

low TSH and high T3 and T4

152
Q

hypothyroid labs

A

high TSH and low T3 and T4

153
Q

thyrotoxic storm labs

A

normal TSH, super high T3 and T4 because brain hasn’t turned TSH off yet - this is an acute problem

154
Q

graves disease

A

primary hyperthyroidism due to autoimmune disease

155
Q

what causes the stimulation of the thyroid in graves disease

A

thyroid stimulating immunoglobulins (TSIs)

156
Q

thyroid stimulating immunoglobulins (TSIs) cause

A

stimulation of the TSH receptor in the gland which results in enlarged gland (goiter) and increased levels of thyroid hormones

157
Q

what does increased levels of thyroid hormone cause

A

sympathetic stimulation- which causes weight loss, tachycardia, heat intolerance, diarrhea, irritability, sleep disturbances

158
Q

signs of graves disease

A

exophthalmos and pretrial myx-edema

159
Q

exophthalmos

A

protrusion of the eyeball from orbital inflammation, edema, and weakness can cause double vision and corneal ulceration

160
Q

diplopia

A

double vision

161
Q

corneal ulceration

A

condition in which inflammation of the outermost layer of the eye results in pain

162
Q

hyperthyroidism treatment

A

antithyroid drugs, surgery - removal of the thyroid, radioactive iodine therapy, beta blockers, and symptom relief

163
Q

thyrotoxic storm

A

life threatening worsening hyperthyroidism in which death can occur within 48 hours if not treated

164
Q

who is at risk for thyrotoxic storm

A

individuals who have undiagnosed graves disease and are subject to excessive medical/physiological or psychosocial stress

165
Q

manifestations of sympathetic crisis of thyrotoxic storm

A

tachycardia, high output heart failure, hyperthermia, agitation, delirium, N/V/D due to fluid depletion

166
Q

thyrotoxic crisis treatment

A

anti thyroid drug, beta blockers for control of cardiovascular symptoms, steroids

167
Q

Hashimoto

A

primary hypothyroidism

168
Q

what causes Hashimoto

A

inflammatory destruction (autoimmune, t lymphocytes, and thyroid autoantibodies) causes thyroid disfunction in which thyroid can’t release or form thyroid hormone

169
Q

manifestation of hypothyroidism

A

low metabolic rate, cold intolerance, lethargy, bradycardia, goiter

170
Q

secondary hypothyroidism causes

A

traumatic brain injury, Subarachnoid hemorrhage, or pituitary tumors or infarction

171
Q

myxedema

A

severe, long-standing, non pitting, boggy edema that can cause loss of mental and physical stamina

172
Q

myxedema coma is caused from

A

hypothyroidism

173
Q

myxedema coma causes

A

decrease LOC, hypotension, hypoglycemia, hypothermia, hypoventilation which causes hypoxia and can lead to lactic acidosis

174
Q

folliculitis

A

infection of the hair follicle that is caused by bacterial, fungal, and viral infection but S. aureus is the predominant culprit

175
Q

treatment for folliculitis

A

soap, water, and topical antibiotics

176
Q

contributing factors of folliculitis

A

moisture, skin trauma, occlusive clothing, poor hygiene

177
Q

furuncles

A

“boils” - folliculitis that is spread to dermal tissue

178
Q

furuncle characteristics

A

deep, firm, red, painful, 1-5 cm, non systemic symptoms, and may drain pus or necrotic tissue

179
Q

main cause of furuncles

A

S. aureus

180
Q

carbuncle

A

collection of infected hair follicles that extends into the subcutaneous tissue

181
Q

characteristics of carbuncle

A

systemic complications - fever, chills, weakness

abscess may develop

182
Q

abscess formation in carbuncles require

A

incision and drainage treated with bacitracin which is a local antibiotic for S. aureus

183
Q

Cellulitis

A

infection of the dermis and subcutaneous tissue usually caused by S. aureus

184
Q

what is needed for cellulitis

A

systemic antibiotic

185
Q

cellulitis can be associated with other diseases including

A

venous insufficiency

186
Q

cellulitis can occur as an extension of

A

a wound as an ulcer, or form furuncles or carbuncles

187
Q

manifestation of herpes zoster

A

pain and paresthesia that affects a dermatome. pain is followed by vesicular eruptions along that dermatome

188
Q

multi-drug resistant organisms

A

MRSA, VRE, ESBL (extended spectrum beta lactates),CRE (carbapenem-resistant Enterobacteriaceae)

189
Q

what helps for multi drug resistant organisms

A

contact isolation, hand washing, good antibiotic stewardship

190
Q

treatment for CRE

A

only 2 antibiotics are able to treat it but one of them had a “all-cause mortality” BBW

191
Q

what happens with a CRE outbreak

A

hospital shutdown - people with infection are sent to a CRE unit

192
Q

When are corticosteroids released from the adrenal cortex? Name 2 of the three key stimuli

A

Low circulating cortisol levels and diurnal patterns of sleep and wake cycle.

193
Q

When is a mineralocorticoid released by the adrenal cortex

A

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.

194
Q

Which two populations may not exhibit the classic signs and symptoms of infection?

A

Geriatric patients or immunocompromised people may not exhibit the classic signs of infection.

195
Q

Patients over the age of 65 may exhibit confusion as a sign

A

infection

196
Q

Identify what must be done before administering empiric antibiotic therapy?

A

Before administering empiric therapy we must obtain blood culture, sputum sample, and a urine sample.

197
Q

You notice your patient is exhibiting itching, throat swelling and a fast irregular pulse. Which three medications would you anticipate administering swiftly

A

Epinephrine, diphenhydramine, and famotidine

198
Q

Identify the group of bacteria that are more difficult to kill and thus can cause more complications.

A

Gram negative bacteria are more difficult to kill leading to them being deadlier.

199
Q

The baseline labs for which two body organs should be assessed before administering most antibiotics?

A

Antibiotics can be hard on the kidney or liver, so kidney and liver labs need to be assessed before administering antibiotics.

200
Q

List the three contributors to one third of all reproductive mortality cases in the U.S.

A

AIDS, genital cancer, and syphilis contribute to one third of all reproductive morality cases.

201
Q

Identify the population most affected by gastric pacemaker cell dysfunction

A

diabetics

202
Q

Identify the 2 main classes of drugs that act on the normal gastric physiology to protect gastric mucosa.

A

Proton pump inhibitors and H2 receptor antagonist

203
Q

Name one response the GI system has to a release of serotonin

A

Serotonin causes vasodilation in the gut.

204
Q

Identify the ABG abnormality associated with vomiting & diarrhea, respectively.

A

Vomiting is associated with metabolic alkalosis and Diarrhea is associated with metabolic acidosis.

205
Q

List the 7 (yes, 7) main functions of the liver.

A
  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
206
Q

The elevation of which liver laboratory test is associated with severe confusion and decreased level of consciousness?

A

Elevated ammonia levels

207
Q

ph of stomach is approximately

A

2

208
Q

what bacteria has evolved to live in acidic environments so it can live in our stomach and cause problems

A

h pylori

209
Q

peristalsis is controlled by

A

pacemaker cells

210
Q

food enters the stomach which stimulates the vagus nerve to

A

release acetylcholine which the stimulates gastrin

211
Q

how does the stomach lining survive through the acidic environment

A

prostaglandins are simulated to secrete mucus that creates a barrier to protect the stomach

212
Q

gastrin inhibition is regulated by

A

somatostatin, secretin, and serotonin

213
Q

too much acid and not enough food in stomach causes

A

endocrine cells of the stomach to release somatostatin

214
Q

food or chyme entering the duodenum does what

A

stimulates the small intestines to secret secretin which promotes release of pancreatic juices and bile from liver to help digest the food

215
Q

neurotransmitter released when food enter into the duodenum

A

serotonin which causes and increase in GI mobility and vasodilation in gut

216
Q

patient who is vomiting or has gastric suction can be seen with a loss of

A

potassium and sodium which can lead to metabolic alkalosis

217
Q

osmotic diarrhea

A

non absorbable substances draw water in- large volume diarrhea can be caused from synthetic sugars or tube feeding

218
Q

secretory diarrhea

A

has both large and small volume diarrhea. can be caused by pathogens or inflammatory disorder

219
Q

motility diarrhea

A

increased motility that causes impaired absorption can be from surgical bypass, IBS, hyperthyroidism, or laxative abuse

220
Q

pt with excessive or chronic diarrhea can end up with

A

metabolic acidosis from the loss of bicarb and other electrolytes

221
Q

bile helps with

A

the breakdown and absorption of fat

222
Q

RBC are broken down into

A

heme and globin but the liver

223
Q

minimum inhibitory concentration

A

lowest amount of antibiotics needed to kill a bacteria includes how long the patient is on and the concentration

224
Q

glucocorticoids and inflammation

A

they are anti-inflammatory because they decrease pattern receptors on macrophages

225
Q

glucocorticoids and immune function

A

immunosuppresant because they decrease distribution T cells and cytokines. they also suppress innate and adaptive immunity so decrease wound healing

226
Q

glucocorticoids and RBC

A

polycythemia (increased RBC) because body is trying to increase O2 carrying capabilities

227
Q

glucocorticoids and fat

A

they increase appetite and cause fat redistribution

228
Q

treatment for inflammatory bowel disease

A

corticosteroids to keep inflammation down now, biologics, immunomodulators- keep inflammation down in future, antibiotics, and treat symptoms -anti-diarrheal and nutritional deficiencies (anemia)

Nursing school level 2 (15 decks)

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