ACUTE 2 FROM GI ON Flashcards
1
Q
Hematemesis
A
vomitting blood
may be red, brown, or black
May look like coffee grounds
A sign of bleeding in the digestive system
Seek medical attention right away
2
Q
hematochezia
A
Passing fresh blood per anus, usually in or with stools
May include bright red blood in the stool or on toilet paper
May also cause abdominal pain, vomiting, or diarrhea
lower***
3
Q
melena
A
Passing black, tarry stools that may have a foul smell
A sign of bleeding in the upper digestive tract
May indicate bleeding in the esophagus, stomach, or first part of the small intestine
upper**
4
Q
Dysfunction
in LES
* Delayed
gastric
emptying
A
GERD
5
Q
Symptoms and/or
complications
resulting from
reflux of gastric
contents into the
esophagus and
more proximal
structures
A
gerd
6
Q
gerd
A
Symptoms and/or
complications
resulting from
reflux of gastric
contents into the
esophagus and
more proximal
structures
7
Q
obesity and hiatal hernias are tied to what clinical presentation/dx of
A
gerd
8
Q
typical signs of gerd
A
heartburn and regurgitation 30-60min after a meal is typical
9
Q
dysphagia and odenophagia are alarming signs of
A
pain and difficultly whne swallowing warning signs of Gerd more serious of gerd
10
Q
Decreased lower esophageal sphincter pressure
A
gerd
11
Q
teach patients with gerd to AVOID
A
AVOID
* Exercise before bed
* Large high fat meals
* Foods that decrease
LES pressure
* Esophageal irritation
* Tight fitting clothes
12
Q
A
13
Q
teach gerd patients to
PROMOTE
A
- Elevate HOB
- Reduce weight
- Eliminate smoking
- Eliminate
exacerbating meds - Use antacids and
alginic acid PRN
14
Q
example of PPI
A
azole
omeprazole
pantoprazole
15
Q
h2 blockers examples
A
famotidine
dine***
16
Q
what is sucralfate used for
A
creates a protectove barrier, used for milder symptoms and can be used safely in pregnancy
17
Q
Epigastric pain
– Burning, aching, hunger-like or gnawing
– 1-3 hours after a meal or at night
– May awaken the patient from sleep
– Relief of pain after eating
– Rhythmic and periodic
* Epigastric tenderness midline or right of
midline
A
duodenal ulcer
18
Q
condition where the normal lining of the esophagus is replaced by a thick, red lining with potential for cancerous changes. It is associated with long-standing gastroesophageal reflux disease (GERD). Although usually asymptomatic, it is a risk factor for esophageal cancer.
A
BARRETTS ESOPHAGUS
19
Q
duodenal ulcer
A
Epigastric pain
– Burning, aching, hunger-like or gnawing
– 1-3 hours after a meal or at night
– May awaken the patient from sleep
– Relief of pain after eating
– Rhythmic and periodic
* Epigastric tenderness midline or right of
midline
20
Q
4X more common
– Age range 30-55
these ulcers occur where
A
Duodenal Ulcers
21
Q
– Seen in lesser
curvature of
stomach
– New cases likely bc
of NSAIDS
– 3-4Xmore prevalent
than duodenal
ulcers in NSAID
users
– Peak age of
incidence is 55-70
yrs
A
Gastric Ulcers
22
Q
Epigastric pain similar to duodenal ulcers
* Pain is NOT usually relieved by food
* Food may precipitate symptoms
* Nausea and anorexia
* Epigastric tenderness at or left of the midline
A
peptic ulcers
23
Q
peptic ulcers
A
Epigastric pain similar to duodenal ulcers
* Pain is NOT usually relieved by food
* Food may precipitate symptoms
* Nausea and anorexia
* Epigastric tenderness at or left of the midline
avoid eating
anemia-gi bleed, or vomiting
lack of responce to PPI
hematemesis or melon
boar dlike abdomen is severe recound tenderness
24
Q
food provokes pain in these ulcers
A
peptic
25
gold standard testing for ulcers
a scope
26
diagnostic for ulcers
50% caused by hpylori
27
hpylori antibodies are
positive for many years
28
fecal hpylori antigen is extremely _____ and can ________
sensitive and done to evaluate treatment efficecy
we should be able to clear h.pylori
96% good sensitivity to discuss and decide treatment
29
hpylori produces what
urease the environment that it lives
acidic environment
30
outpatient diagnostic for hpylori
drink the carbon labeled urea breath drink and they ingest it, the urease enzyme actually splits the isotope and the co2 levels goes up and they breath into a bag before and then drink the dirnk and thenbreath again and if they have it it will go up the co2 leevels.
31
Triple therapy for hpylori
C + A/M + ALWAYS A PPI
Triple Therapy 10- to 14-days
* Clarithromycin 500 mg bid
– Plus
* Amoxicillin 1 g bid
– Or
* Metronidazole 500 mg bid
– Plus
* A PPI (Omeprazole)
32
hallmark left lower quadrant pain
diverticultiis
33
borborygmi
hyperactive sounds
34
differentiate level of severity mild to moderate disease treatment for chrons
aminosalicylates
steriods-mild short periods and then maintenance dosages
oral mild IV hydrocort, severe?
immunomodulating drigs moderate to severe -maintain remission
biologic therpay-newer drugs make sure you know monoclonal antitumor necorsis factor a phase inflammatory cascade that is blocked, patients that get put on refractory to sever neot first line,t ehy will help in two weeks*******
35
mild outpatient treatment this is not indicated
antibitoics*** haha my dad wants this all the time, not first line choice; only if they are delicate immunocompromised.
36
Moderate to severe CD treatment
immunimodulating drugs and or biolgoic therpay
37
perforation hallmark clinical presentation
rigid, absent bowel sounds, hypoactive or no bowel sounds, rebound tenderness
38
rectal bleeding and frequency of stools, colicky wave pain, up to ten stools a day during an exacceration colicky wave like pain, blood in stool what is this?
ulcertive colitis
39
all autoimmune response we see this commonly
fever
40
msyk the dx of ulcerative colitis
a scope, but not in the middle of a flare.
41
diagnostics of ulcertive colitits we see what
esr-elevated, crp-elevated, cmp lfts, albumin, cbc
42
what questionnaire is used for ulcertive colitis
mayo score
43
FC is what in uc treatment/diagnositc?
increased in exaccerabations helps to idenfity treatment progression a noninvasive marker of disease activity, involves neurtorphils
44
3 loose stools in 24 hours, watery diarrhea we are thinking?
cdiff
45
xray what are you looking at in the belly
dilating loops
46
Toxic megacolon?
greater than 6
47
appendicitis classic signs
rlq- sometimes it starts gastric, periumbilic pain n/v rebound tenderness, rigicity-
mcburney point***
48
mc burney point
2/3 of the belly button and iliac********************************
49
rovsigns referred pain?
palpate the left sign the pain radiates to the right side of the
50
Psoas signs
pulling on the right lowerin quardant
51
obturator sign
bringing the leg towards
52
mechanical versus nonmechanical obstruction
nonmechanical like an ileus- shut down flow is ceased, not innerved to move the pertilasis along versus an actual obstruction is something in the way
53
overt gi bleeding
bleeding refers to visible bleeding from the digestive tract. It is a medical emergency that requires prompt medical attention.
54
occult bleeding
need to test for it
55
obscure bleeding
negative endoscopy but they are still bleeding
56
type and causes of UGI
ulcer disease nsaid use chronic alcohol use heptitiat and or boerhaave syndrome
57
type of lower GR bleeding
anatomic-diverticulosis, vascular, neoplasm, inflammatory non infections chrons disease and or an infectios like salmonella
58
examination of the stool if it is upper or lower- you see hematemsis what are you thinking?
ugi-almost certain
lower rare
59
examination of the stool if it is upper or lower; melena
propbable UGI and possible LGI
60
examination of the stool if it is upper or lower- blood streaked stool
rare for UGI and almost certain it is lower
61
need to know????guiac test why and interfereance
the better test FIT, react to the hemo?
62
national standards or practice
The International Consensus on Upper
Gastrointestinal Bleeding Conference Group
recommendations for Management of Upper
GI Bleeding:
* Early identification of high-risk patients can
facilitate appropriate intervention, which
minimizes morbidity and mortality.
* Use of a prognostic tool
63
Screening tool to assess the likelihood that a
patient with an acute GI bleed will need to
have medical intervention (blood transfusion
or endoscopy
glasgow-blatchford scare
64
msyk-likely a gi bleed the glasgow-blatchford score
Screening tool to assess the likelihood that a
patient with an acute GI bleed will need to
have medical intervention (blood transfusion
or endoscopy
65
management of a GI bleed msyk what to do
Monitor hemodynamic status
– Cardiac monitoring
– Strict I&O
– Type & Cross 2-4 U PRBCs
* Consider labs in pedi tubes
* NG tube placement / suction / lavage
* Pharmacological therapy
* Endoscopy
Volume replacement
– 2 large bore IV’s or central line
– NS fluid of choice/Packed RBC
transfusion
* Pressor therapy
* O2 administration
* Correction of coagulopathy
* Endotracheal Intubation
* Risk Stratification
66
what is the hgb goal for a gi bleed
>7
67
variceal hemorrhage what drugrs do you use?
octrotide & vasopressin
68
reduces
portal blood blow flow thereby
reducing variceal pressures and
promoting hemostasis
octreotide (sandostatin)
69
Directly constricts
mesenteric arterioles and
decreases portal venous inflow
vasopressin
70
Generic term for end
stage liver disease
* Characterized by
hepatocytes and
replacement of normal
hepatic architecture
with fibrotic tissue and
regenerative nodules
cirrhosis
71
cirrhosis
Generic term for end
stage liver disease
* Characterized by
hepatocytes and
replacement of normal
hepatic architecture
with fibrotic tissue and
regenerative nodules
72
hepatic encephalopathy msyk management
Lactulose/Rifampin/Neomycin, Flagyl
- Protein restriction
- Coagulopathy
- Vitamin K
- FFP
- Prevent bleeding
73
acidotic fluid
with >250 neutrophils/mL
– sensitivity of 93% and specificity of 94%
* Common organisms are
– E. Coli
– Klebsiella
– Strep. Pneumoniae
* Polymicrobial infection is uncommon and
should lead to the suspicion of secondary
bacterial peritonitis
74
empiric antibiotic therapy liver patients* spontaneous bacterial peritonitis the fluid from when you tap it what are you going to give
3rd Generation Cephalosporin
* Ceftriaxone 1 g IV daily
* Cefotaxime 1 to 2 g IV q6-8hr
– Albumin 1.5g/kg body weight at time of diagnosis
and 1.0g/kg body weight on day 3 improves
survival and prevents renal failure in SBP.
75
meld score is used for
transplanted, unos
The MELD equation that is currently used by
UNOS for prioritizing allocation of deceased
donor livers for transplantation
76
alcoholic cirrhosis questionnaire the score______
meld
77
steatosis with inflammation, with
hepatocyte injury
NASH
NONALCOHOLIC FATTY LIVER
Nonalcoholic steatohepatitis
78
MANAGMENT OF NASH, Nonalcoholic steatohepatitis
Lifestyle modifications
– Weight loss
– Exercise
– Reduce cholesterol
– Protect liver
* Medications
– Vitamin E
* Bariatric surgery
* May need liver transplant
79
LAB DIAGNOSTICS FOR HEPATITIS AST AND ALT?
10-100 FOLD INCREASE
80
LAB OF HEPATITIS BILIRUBIN?
Bilirubin moderately increased 5-10mg/dL or even
markedly increased at 15-25mg/dL
81
HALLMARK OF LOSS OF SYNTHETIC FUNCTION OF THE LIVER TAKING A HIT
COAGS GO UP
PT/INR useful is assessing the degree of synthetic
dysfunction
82
IGG- IG GONE IS FOR WHAT?
HEPATITIS A LIFELONG PROTECTION AGAINST THE DISEASE
83
SEROLOGIES FOR HEPAITTIS A
IGM
ACTIVE
84
ANTIHAV FOR HEP A
ANTIBIOIDES YOU AR ELOOKING FOR FOR ACTIVE HEPAITTIS
85
SEROLOGIES FOR HEPATITIS A
IGG
RECOVERED
86
Anti HAV + IgM=active hepatitis
IgM antibodies usually appear during the first
week of symptomatic disease and slowly decline
over a period of 3-4 months
87
IgM antibodies usually appear during the first
week of symptomatic disease and slowly decline
over a period of 3-4 months
Anti HAV + IgM=active hepatitis
88
Peak levels of IgG antibodies occur after 1 month
of illness and may persist for life: they provide
long term protective immunity against reinfection
Anti HAV + IgG=recovered infection or immunity
89
Anti HAV + IgG=recovered infection or immunity
Peak levels of IgG antibodies occur after 1 month
of illness and may persist for life: they provide
long term protective immunity against reinfection
90
HIGHLY CONTAGIOUS HEPTITIS
B
91
PEOPLE AT RISK FOR HEP B
Household contacts of persons
with chronic HBV infection
* Health care and public safety
workers at risk for
occupational exposure to
blood or blood-contaminated
body fluids
* Hemodialysis patients
* Residents and staff of facilities
for developmentally disabled
persons
* Travelers to countries with
intermediate or high
prevalence of HBV infection
92
HEP B SURFACE ANTIGEN CHART PAGE 41*****
93
IS THERE A CURE FOR HEP B?
NO GOAL IS TO SUPRESS THE VIRUS AND PRVENT LIVER INJURY
94
MUST KNOW HEP C ANTIBODIES
WE CAN TEST
95
IMPORTNACE OF GENOTYPING
WE DO REALLY GENOTYPE WE WOULD GENOTYPE IF THEY FAILED TREATMENT
96
LIPASE ELVEATED IS A MARKER OF
ACUTE PANCREATITITS
97
pancreatitis necrotizing is found on what type of diagnostic test
CT
98
murphy sign
take a deep breath and palpate cause pain for cholecystitis
99
1st test for gallbladder
ultrasound
100
treatment for gallstones
bile acid therapy ursodol (actigall)
could take 3 months to 2 years to get rid of gallstone, prevent formation of stones, candiiates that are going to keep their gallb..adder
stones composed of cholesterol
101
acute cholangitis
bacterial infection super imposed on a biliary onstruction and can be relatedto a tumor/cancer
can also happen after an ercp.
bacterial enters from the duodenum
102
charcots triad
right upper quadrant pain, fever with chills and jaundice
103
infection of the biliary tree and bacteremia
acute cholangitis
104
Nephrotic:
Nephrotic:
Profound proteinuria
Hypoalbuminemia
Edema
Immune complex deposits: Epithelial
NO cellular inflammatory reaction
105
Nephritic:
Nephritic:
Variable proteinuria
Azotemia
Hematuria
Immune complex deposits
Cellular inflammatory reaction
106
most common cause of ESRD in the US
diabetic nephropathy
107
AKI is acute _____ to ______
The decline of renal function over hours to days with the resultant increase of nitrogenous wastes such as urea and creatinine in the blood.
108
diabetic nephropathy
persistent albuminuria >300mg that is confirmed on at least 2 occasion 3-6 months apart; treatment aggressive control of glucose and blood pressure.
109
The hallmark of AKI is
progressive azotemia accompanied by metabolic derangements such as metabolic acidosis and hyperkalemia and volume overload
110
pre renal
sudden and sever drop in bp shock, loss of volume, interruption of blood flow to the kidney from severe injury or illness
hepatorenal syndrome, massive heart attack not pumping to the kidneys, chf exacerbation, shock state hypovolemia, sepsis and or cardiac failure
could be stenosis causing decrease flow to the kidney
loss of volume or perfusion
111
intral renal
direct damage to the kidneys by inflammation toxins drugs infection ro reduced blood supply
if its prolonged enough then will cause, prolonged time- assume damage is now done intra renally
nsaids would really cause intrarenal causes
112
post renal
sudden obstruction*** of the urine flow
due to enlarged prostate or kidney stones, bladder tumor, and or overall injury
113
assessment for prerenal causes
thirst, orthostatic, low bp, dry mucus, dec turgor, tachycardia, redcued jvp, n/v
114
if you have damage to the kidney itself like ATN glomerulonephritis is a form of _____ ARF
intrarenal
115
intra renal assessment
Fever, arthralgias , rash, flank pain, digital ischemia,
Oliguria, edema, hypertension and active urine sediment may indicate acute glomerulonephritis of vasculitis
Papilledema, neurologic dysfunction and LVH associated with malignant HTN leading to ARF
116
a prolonged hypoperfused state can lead to
ATN
acute tubular necrosis
117
This is the phase during which the injury that leads to ARF occurs.
Initiation:
118
The _______ phase is when your urine output is low.
Oliguric
119
what are the phases of ARF is knowing this important?
onset, oliguria, diuretic, recovery
120
The ________ phase is characterized by a marked increase in your urine output as your kidney function starts to return.
Diuretic
121
The __________ phase is when your kidney function begins to stabilize.
Recovery
122
FENa
calculation determines the degree of ARF pre, intra, and or post renal failure
should be <1%
we should be able to reabsorb
123
FENa>1% means
Damage to the kidney itself intratenal
124
FENa incorporate what to get the calculation?
urine sodium, urine creatinine, plasma sodium and plasma creatinine
125
INDICATIONS FOR ACUTE HD AEIOU
ACIDOSIS
ELECTROLYTE ABNORMALITIES
INGESTION OF SUBSTANCES
OVERLOAD OF FLUID
UREMIA/UREMIA SYMPTOMS PERICARDITIS, ENCEPHALOPATHY
126
HIGH BUN WHAT KIND OF DIET DO THEY FOLLOW
LOW PROTEIN DIET
ONCE IT GETS BETTER WE CAN GIVE THEM PROTEIN INTAKE***
127
TREATING PATHOLOGIC MANIFESTATIONS: ANEMIA
TREAT WHEN HGB IS BELOW 10 AND TREAT WITH ERYTHROPOIESIS-STIMULATING AGENTS
128
TREATING PATHOLOGIC MANIFESTATIONS: HYPERPHOSPHATEMIA
TREAT WITH DIETARY PHOSPHATE BINDERS AND DIETARY PHOSPHATE BINDERS AND PHOSPHATE RESTRICTIONS
129
TREATING PATHOLOGIC MANIFESTATIONS: HYPOCALCEMIA
GIVE CALCIUM SUPPLEMENTS WITH OR WITHOUT CALCITROL
130
TREATING PATHOLOGIC MANIFESTATIONS: HYPERPARATHYROIDISM
TREAT WITH CALCITROL, VITAMIN D ANALOGES OR CALCIMIMETICS
