332 test 2 Flashcards
1
Q
what secretion increases when you eat and during stress
A
gastrin secretion
2
Q
what does gastrin do?
A
stimulates gastric glands to secrete HCl, pepsinogen, and histamine
3
Q
what stimulates histamine to be released in mucosa of stomach
A
gastrin
4
Q
what does histamine in the stomach do
A
stimulates acid secretion
5
Q
what stimulates acetylcholine in the stomach
A
vagus and local nerves in the stomach
6
Q
what does acetylcholine do to the stomach
A
stimulates the release of pepsinogen and acid secretion
7
Q
what do prostaglandins do
A
regulate perfusion to stomach, regulates mucus to release bicarb, and controls acid amount secreted by parietal cells
8
Q
what do the parietal cells do
A
secrete HCl and intrinsic factor
9
Q
what do chief cells do
A
release pepsinogen to breakdown protein
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
11
Q
what is intrinsic factor needed for
A
absorption of B12
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
13
Q
risk factors to gastritis/peptic ulcer disease
A
alcohol, stress, caffeine, fatty meals, NSAID use, H. Pylori, smoking (vaping)
14
Q
Gastritis
A
inflammatory erosion in the stomach related to increased HCl
15
Q
not considered an ulcer until
A
erosive factors that have overcome protective factors get deep enough to hit the bloodstream
16
Q
is gastritis does not resolve it can turn into
A
chronic gastritis or peptic ulcer disease
17
Q
signs and symptoms of gastritis
A
epigastric pain, nausea, vomiting, GI bleeding
18
Q
chronic gastritis can cause
A
pernicious anemia
19
Q
what is pernicious anemia
A
anemia due to low B12 absorption
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
21
Q
treatment for gastritis
A
soft bland diet, but if from h. Pylori should take antibiotics
22
Q
what lab do you want to pay attention to with gastritis
A
H&H
23
Q
what meds can people take for gastritis
A
PPIs or H2 blockers
24
Q
what happens to the GI mucosa in peptic ulcer disease
A
the GI mucosa is digested by pepsin
25
NSAIDs do what
block prostaglandin synthesis
26
Zollinger Ellison syndrome
syndrome associated with peptic ulcer disease caused by neuroendocrine gastrin secreting tumor which causes excess secretion of gastric acid
27
treatment for H. pylori
PPI and antibiotic
28
which type of ulcers occur more often
duodenal ulcers
29
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
30
peptic ulcer disease can lead to high risk of
gastric cancer
31
sign and symptoms of duodenal ulcer
pain 2-3 hours after eating and in the middle of the night
32
sign and symptoms or gastric ulcer
pain right after eating
33
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
34
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
35
secretin does what
influences the environment of the duodenum by regulating secretions in the stomach, pancreas, and liver.
36
what can affect the effectiveness of H2 receptor antagonist
smoking
37
H2 receptor antagonist do what
decrease acetylcholine and gastrin. increases the ph and reduces the H+ secretion from the parietal cells
38
example of H2 receptor antagonist
famotidine (Pepcid)
39
what other drugs should not be given with H2 receptor antagonist
drugs that need to be broken down because of the decreased amount of gastric acid so it will mess with the absorption
40
nursing consideration for Pepcid
dilute with 5-10 ml of NS and push over 2 minutes or can cause hypotension
41
where is the vomiting center
in the brain
42
what causes vomiting sensation
neurotransmitter stimulate chemoreceptor trigger zone
43
should you drink water right after vomiting
no inhibit it for 30 minutes after
44
what drugs can be used as adjust with nausea and vomiting
dexamethasone and lorazepam
45
liver metabolizes
glucose and stores it as glycogen and converts glycogen to glucose
46
what happens with glucose in liver disease patients
they can get hepatic diabetes from chronic high blood glucose levels
47
what is the byproduct of protein metabolism
ammonia
48
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
49
liver stores
vitamins B12, A, C, E, D, and K
50
vitamin D does what
helps absorb calcium
51
vitamin K does what
helps the clotting process
52
liver helps with the production of
blood plasma proteins
53
portal hypertension
abnormally high blood pressure in the portal venous system caused by resistance to blood flow
54
where does the blood in the hepatic portal vein come from
all the organs that play a role in digestion so the stomach, spleen, pancreas, and intestines
55
intrahepatic causes of portal hypertension
inflammation, fibrosis, and vascular remodeling that occur from cirrhosis or hepatitis
56
post hepatic causes of portal hypertension
impaired pumping of the heart or obstruction from Right HF or thrombus
57
consequences of long term portal hypertension
varices, splenomegaly, hepatopulmonary syndrome, portopulmonary hypertension
58
varices
distended veins from obstruction/pressure. blood then is shunted and pushed into other areas including the abdominal wall, stomach and esophagus
59
why are varies life threatening
because the vessels can rupture and lose a lot of blood
60
splenomegaly
enlarged spleen caused by increased pressure in the splenic vein which branches from the portal vein
61
most common symptom of splenomegaly
thrombocytopenia (low platelets)
62
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
63
portopulmonary hypertension
the pressure buildup in the portal vein causes remodeling and pulmonary vasoconstriction
64
ascites
accumulation of fluid in the peritoneal cavity
65
most common cause of ascites
cirrhosis
66
factor that contribute to the development of ascites
decreased synthesis of albumin by the liver, portal hypertension, and splanchnic arterial vasodilation
67
what do decreased albumin levels and portal hypertension do to pressure gradient
cause capillary hydrostatic pressure to exceed capillary osmotic pressure which pushes water into the peritoneal cavity (ascites)
68
what is splanchnic arterial vasodilation associated with
increased production of nitric oxide by a diseased liver
69
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
70
goal for ascites
palliative care (comfort) this can include paracentesis
71
what to watch out for during paracentesis
taking off too much fluid can cause the patient's blood pressure to drop dramatically
72
hepatic encephalopathy
complex neurologic syndrome where toxins effect neurotransmission because the liver is not able to convert ammonia to urea in its toxic state
73
symptoms of hepatic encephalopathy
range from lethargy to coma
74
what can hepatic encephalopathy cause
astrocyte swelling from elevated ammonia levels, altered Blood brain barrier, and cerebral edema
75
treatment for hepatic encephalopathy
fluid and electrolyte maintenance, cessation of depressant drugs, protein restriction
76
jaundice results from either
obstructive or hemolytic cause
77
obstructive cause of jaundice can either be
extrahepatic or intrahepatic
78
extrahepatic causes of jaundice
liver still working but bilirubin accumulation because gallstone blockage of bile flow- considered conjugated
79
conjugated
hepatocytes functioning so something else is causing the problem
80
unconjugated
hepatocytes not functioning so they are the cause of the problem
81
intrahepatic cause of jaundice
hepatocyte dysfunction so liver has decreased ability to excrete bilirubin
82
hemolytic cause of jaundice
excesses hemolysis of red blood cells and liver can't keep up with the amount of RBC that need to be recycled
83
liver labs will be normal in what type of jaundice
extrahepatic jaundice
84
hepatorenal syndrome
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
85
cause of hepatorenal syndrome
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
86
cirrhosis
irreversible, inflammatory, and fibrotic liver disease
87
causes of cirrhosis
hepatitis a/b/c, right HF, alcohol, autoimmune/hereditary, and idiopathic (unknown)
88
structural changes in cirrhosis are caused by
injury from viruses/toxicity from alcohol and fibrosis
89
fibrosis in the liver of cirrhosis patients is a consequence of
infiltration of leukocytes and release of inflammatory mediators
90
nonalcoholic fatty liver disease is associated with
obesity, high triglycerides, and DM 2
91
nonalcoholic fatty liver disease signs and symptoms
often asymptomatic for years because it progresses slowly
92
the most severe forms of nonalcoholic fatty liver disease will progress to
cirrhosis and end stage liver disease
93
inflammatory bowel disease includes
ulcerative colitis and crohns
94
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
95
inflammation in ulcerative colitis vs Crohn's
inflammation in ulcerative colitis is in the mucosal layer while Crohn's involves the entire intestinal wall
96
clinical manifestations in ulcerative colitis vs Crohn's
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
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
98
out of ulcerative colitis vs Crohn's which can form into abscesses and necrosis and which can form into anal fistulas, obsesses, and obstructions
ulcerative colitis can form into abscesses and necrosis and Crohn's can form into anal fistulas, obsesses, and obstructions
99
chronic inflammatory bowel diseases are diseases of
remission and exacerbations
100
chronic inflammatory bowel diseases increase risk for
cancer - ulcerative colitis had a higher risk than Crohn's
101
causes of constipation
dehydration, suppression of the urge to go, impaired colonic motor activity, pelvic floor/anal dysfunction, drugs, endocrine disorders, aging, pregnancy, and colorectal cancer
102
what would cause a patient to have pelvic floor/anal dysfunction
neurogenic disorders such as paralysis
103
what would cause a patient to have impaired colonic motor activity
a low residual diet (low fiber)
104
what drugs cause constipation
opioids, calcium or aluminum antacids, anticholinergics, and iron
105
endocrine disorders that can cause constipation
hypothyroidism and DM
106
ways to treat constipation
dietary, behavior, pharmacological including enemas, and if really ban through surgery
107
excessive cortical =
Cushing syndrome
108
excessive ACTH
Cushing disease
109
anemia in ulcerative colitis vs Crohn's
ulcerative colitis can have blood loss anemia vs Crohn's can have macrocytic anemia from low B9 and B12 absorption
110
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
111
cause of cushing disease
caused by a tumor either in pituitary or adrenal
112
cause of Cushing syndrome
excessive/long term steroid use or can happen in people with long term high levels of stress
113
what are two things that occur in people with hypercortisolism aka cushings syndrome
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
hormonal regulation occurs in response to
chemical factors, endocrine factors, or control from the nervous system in response to stimuli
115
negative feedback loop of hormones
occurs when there is a neural, chemical, or endocrine response to stimulus that decreases the synthesis and secretion of a hormone
116
stress hormones do what to our BP and glucose
they are vasoconstrictors so will increase BP and increase blood glucose levels
117
adrenal cortex secretes
corticosteroids in response to low circulating cortisol levels, diurnal patterns of wake and sleep, and stress
118
endogenous glucosorticoid =
cortisol
119
endogenous mineralocorticoid
aldosterone
120
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).
121
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
122
mineralocorticoid function
sodium retention, potassium/H+ loss, BP control, increase cardiac contraction, increase systemic vascular resistance, and decrease fibrolysis
123
how do glucocorticoids promote carbohydrate metabolism
by promoting gluconeogenesis in the liver and decreasing glucose uptake thus promoting insulin resistance
124
calcitonin is secreted by the thyroid when
circulating calcium levels are too high
125
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
126
what is required for the synthesis of T3 and T4
iodine
127
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
128
calcitonin function
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
what happens with weight during cushing syndrome
weight gain with a redistribution of fat
130
what happens with glucose in Cushing syndrome
glucose intolerance occurs because of cortisol induces insulin resistance and increased gluconeogenesis
131
what does cortisol induces insulin resistance cause
polyuria and glycosuria and 20% of individuals with Cushing syndrome will develop DM
132
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
133
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
134
bone wasting causes
increase fracture risk, increase risk of osteoporosis, hypercalciuria, and risk of stones
135
if you have hypercalciuria then you most likely have
hypocalcemia
136
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
137
what does increased adrenal androgen do to the body
can cause symptoms of virilization
138
virilization
taking on the characteristics of men such as increased hair growth...
139
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
140
without treatment for cushing syndrome
50% of patients die within 5 years due to infection, HTN, or suicide
141
hyposecretion of cortisones and aldosterone
Addison disease
142
Addisons disease is caused by
autoimmune mechanism that destroy adrenal cells
143
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
144
usually don't see the signs and symptoms of Addisons until
90% of the adrenocortical tissue is destroyed
145
what causes the hypo section or steroids in Addisons disease
inadequate stimulation and inadequate synthesis of the steroids
146
signs and symptoms of Addison disease
weight loss, fatigue, N/V/D, skin changes, infection
147
treatment of Addison disease
lifetime fludrocortisone and glucocorticoid, a minimum of 3400 mg of sodium per day, and low stress
148
adrenal crisis can be caused by
Addison disease or stopping exogenous steroids too fast
149
what occurs during an adrenal crisis
hypotension, vascular collapse, hypovolemic shock
150
priority treatment for Adrenal crisis
administer cortisol
151
hyperthyroid labs
low TSH and high T3 and T4
152
hypothyroid labs
high TSH and low T3 and T4
153
thyrotoxic storm labs
normal TSH, super high T3 and T4 because brain hasn't turned TSH off yet - this is an acute problem
154
graves disease
primary hyperthyroidism due to autoimmune disease
155
what causes the stimulation of the thyroid in graves disease
thyroid stimulating immunoglobulins (TSIs)
156
thyroid stimulating immunoglobulins (TSIs) cause
stimulation of the TSH receptor in the gland which results in enlarged gland (goiter) and increased levels of thyroid hormones
157
what does increased levels of thyroid hormone cause
sympathetic stimulation- which causes weight loss, tachycardia, heat intolerance, diarrhea, irritability, sleep disturbances
158
signs of graves disease
exophthalmos and pretrial myx-edema
159
exophthalmos
protrusion of the eyeball from orbital inflammation, edema, and weakness can cause double vision and corneal ulceration
160
diplopia
double vision
161
corneal ulceration
condition in which inflammation of the outermost layer of the eye results in pain
162
hyperthyroidism treatment
antithyroid drugs, surgery - removal of the thyroid, radioactive iodine therapy, beta blockers, and symptom relief
163
thyrotoxic storm
life threatening worsening hyperthyroidism in which death can occur within 48 hours if not treated
164
who is at risk for thyrotoxic storm
individuals who have undiagnosed graves disease and are subject to excessive medical/physiological or psychosocial stress
165
manifestations of sympathetic crisis of thyrotoxic storm
tachycardia, high output heart failure, hyperthermia, agitation, delirium, N/V/D due to fluid depletion
166
thyrotoxic crisis treatment
anti thyroid drug, beta blockers for control of cardiovascular symptoms, steroids
167
Hashimoto
primary hypothyroidism
168
what causes Hashimoto
inflammatory destruction (autoimmune, t lymphocytes, and thyroid autoantibodies) causes thyroid disfunction in which thyroid can't release or form thyroid hormone
169
manifestation of hypothyroidism
low metabolic rate, cold intolerance, lethargy, bradycardia, goiter
170
secondary hypothyroidism causes
traumatic brain injury, Subarachnoid hemorrhage, or pituitary tumors or infarction
171
myxedema
severe, long-standing, non pitting, boggy edema that can cause loss of mental and physical stamina
172
myxedema coma is caused from
hypothyroidism
173
myxedema coma causes
decrease LOC, hypotension, hypoglycemia, hypothermia, hypoventilation which causes hypoxia and can lead to lactic acidosis
174
folliculitis
infection of the hair follicle that is caused by bacterial, fungal, and viral infection but S. aureus is the predominant culprit
175
treatment for folliculitis
soap, water, and topical antibiotics
176
contributing factors of folliculitis
moisture, skin trauma, occlusive clothing, poor hygiene
177
furuncles
"boils" - folliculitis that is spread to dermal tissue
178
furuncle characteristics
deep, firm, red, painful, 1-5 cm, non systemic symptoms, and may drain pus or necrotic tissue
179
main cause of furuncles
S. aureus
180
carbuncle
collection of infected hair follicles that extends into the subcutaneous tissue
181
characteristics of carbuncle
systemic complications - fever, chills, weakness
| abscess may develop
182
abscess formation in carbuncles require
incision and drainage treated with bacitracin which is a local antibiotic for S. aureus
183
Cellulitis
infection of the dermis and subcutaneous tissue usually caused by S. aureus
184
what is needed for cellulitis
systemic antibiotic
185
cellulitis can be associated with other diseases including
venous insufficiency
186
cellulitis can occur as an extension of
a wound as an ulcer, or form furuncles or carbuncles
187
manifestation of herpes zoster
pain and paresthesia that affects a dermatome. pain is followed by vesicular eruptions along that dermatome
188
multi-drug resistant organisms
MRSA, VRE, ESBL (extended spectrum beta lactates),CRE (carbapenem-resistant Enterobacteriaceae)
189
what helps for multi drug resistant organisms
contact isolation, hand washing, good antibiotic stewardship
190
treatment for CRE
only 2 antibiotics are able to treat it but one of them had a "all-cause mortality" BBW
191
what happens with a CRE outbreak
hospital shutdown - people with infection are sent to a CRE unit
192
When are corticosteroids released from the adrenal cortex? Name 2 of the three key stimuli
Low circulating cortisol levels and diurnal patterns of sleep and wake cycle.
193
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.
194
Which two populations may not exhibit the classic signs and symptoms of infection?
Geriatric patients or immunocompromised people may not exhibit the classic signs of infection.
195
Patients over the age of 65 may exhibit confusion as a sign
infection
196
Identify what must be done before administering empiric antibiotic therapy?
Before administering empiric therapy we must obtain blood culture, sputum sample, and a urine sample.
197
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
198
Identify the group of bacteria that are more difficult to kill and thus can cause more complications.
Gram negative bacteria are more difficult to kill leading to them being deadlier.
199
The baseline labs for which two body organs should be assessed before administering most antibiotics?
Antibiotics can be hard on the kidney or liver, so kidney and liver labs need to be assessed before administering antibiotics.
200
List the three contributors to one third of all reproductive mortality cases in the U.S.
AIDS, genital cancer, and syphilis contribute to one third of all reproductive morality cases.
201
Identify the population most affected by gastric pacemaker cell dysfunction
diabetics
202
Identify the 2 main classes of drugs that act on the normal gastric physiology to protect gastric mucosa.
Proton pump inhibitors and H2 receptor antagonist
203
Name one response the GI system has to a release of serotonin
Serotonin causes vasodilation in the gut.
204
Identify the ABG abnormality associated with vomiting & diarrhea, respectively.
Vomiting is associated with metabolic alkalosis and Diarrhea is associated with metabolic acidosis.
205
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
206
The elevation of which liver laboratory test is associated with severe confusion and decreased level of consciousness?
Elevated ammonia levels
207
ph of stomach is approximately
2
208
what bacteria has evolved to live in acidic environments so it can live in our stomach and cause problems
h pylori
209
peristalsis is controlled by
pacemaker cells
210
food enters the stomach which stimulates the vagus nerve to
release acetylcholine which the stimulates gastrin
211
how does the stomach lining survive through the acidic environment
prostaglandins are simulated to secrete mucus that creates a barrier to protect the stomach
212
gastrin inhibition is regulated by
somatostatin, secretin, and serotonin
213
too much acid and not enough food in stomach causes
endocrine cells of the stomach to release somatostatin
214
food or chyme entering the duodenum does what
stimulates the small intestines to secret secretin which promotes release of pancreatic juices and bile from liver to help digest the food
215
neurotransmitter released when food enter into the duodenum
serotonin which causes and increase in GI mobility and vasodilation in gut
216
patient who is vomiting or has gastric suction can be seen with a loss of
potassium and sodium which can lead to metabolic alkalosis
217
osmotic diarrhea
non absorbable substances draw water in- large volume diarrhea can be caused from synthetic sugars or tube feeding
218
secretory diarrhea
has both large and small volume diarrhea. can be caused by pathogens or inflammatory disorder
219
motility diarrhea
increased motility that causes impaired absorption can be from surgical bypass, IBS, hyperthyroidism, or laxative abuse
220
pt with excessive or chronic diarrhea can end up with
metabolic acidosis from the loss of bicarb and other electrolytes
221
bile helps with
the breakdown and absorption of fat
222
RBC are broken down into
heme and globin but the liver
223
minimum inhibitory concentration
lowest amount of antibiotics needed to kill a bacteria includes how long the patient is on and the concentration
224
glucocorticoids and inflammation
they are anti-inflammatory because they decrease pattern receptors on macrophages
225
glucocorticoids and immune function
immunosuppresant because they decrease distribution T cells and cytokines. they also suppress innate and adaptive immunity so decrease wound healing
226
glucocorticoids and RBC
polycythemia (increased RBC) because body is trying to increase O2 carrying capabilities
227
glucocorticoids and fat
they increase appetite and cause fat redistribution
228
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)
