Case study Cram (-; Flashcards
WBC
4-10.5
RBC
3.8-5.2
HgB
120-150
HCT
0.38-0.48
PT-INR
0.9-1.1
platelet
150-400
Neutrophil
2-6
Na
135-145
K
3.5-5
glucose
3.9-11
creatinine
50-90
GFR
> 60
PTT
23-32
what could polycythemia mean
increased RBC so hypoxia, tumour, dehydration, kidney tutor
what could anemia mean
bleed, renal failure, malnutrition, iron deficiency, over hydration
why do we get HgB
CBC (complete blood count) bleeding, surgery, kidney disease, cancer treatment
what would low HgB mean
anemia, bleeding, chronic kidney disease, cancer treatment, rheumatoid arthritis
what would hi HgB mean
COPD, lung scaring, HF d/t chronic hypoxia
what is HCT
%RBC in blood
what is low HCT
anemia, nutritional deficiency, CKD, leukaemia
what would hi HCT mean
dehydration, lung disease, CAD
what does neutrophilia mean
acute bacterial infection, inflammation (RA_, tissue death (sx, MI, Burn) stess
what does neutropenia mean
sepsis, reaction to drugs, autoimmune
hat does lymphocytosis mean
viral infection, lymphocytic leukaemia
what doe lympopenia mean
autoimmune (RA) infection, bone marrow dmg, immune disease
why test NA
general malaise, dehydration, vomiting, monitor in (HTN, HF, Chronic liver disease & kidney disease)
what would cause hyponatremia
diarrhea, vom, diuretics, increased H2O, chronic kidney disease, malnutrition, heart failure
what would cause hyper natremia
usually dehydration
why is K+ tested
kidney disease, weak muscles, arrhythmia, diuretics, HTN med
what would cause hyperkelemia
kidney disease, tissue dmg, infection, diabetes, dehydration, drugs
what would cause hypokalemia
diuretics, diarrhea, vomiting, diabetes
what is creatinine
waste product removed by kidneys
what does high creatinine mean
kidney disease, UTI, infection, decreased blood flout kidneys
what does thrombocytopenia mean
not enough made or there has been distruction
cancer treatment, drugs, autoimmunity
bleeding risk
what does thrombocytosis mean
hemolytic anemai, iron deficiency, surgery, trauma, infection, medication, spleen removal, blood clots
what does troponin elevation mean
even slight increase means Heart damage
may also be d/t medical procedure, cardiomyopathy of HF
when would you test BNP
symptoms of HF (SOB, EDEMA)
what does it mean when BNP is high
heart cannot pump the way it should
most likely HF or (KF, PE, Pulm HTN, sepsis, lung problems)
it is a hormone secreted by cardiomyocytes in the ventricles in response to increased streching cause by increased blood volume
what is PTT
partial thromboplastin time - measures time it takes for a clot to form - an tell if clotting factors are working
why would you test PTT:
unexplained bleeding, bruising, clouting, liver disease, surgery, HEPARIN
LOOKING AT EXTRINTRINSIC & COMMON PATH
why would PTT be longer than normal
bleeding disorder, liver disease, lupus, vitamin K deficiency
why is PT INR tested
detect blleeed/ clot disorder - INR to determine how well anticoagulant warfarin is working (INTRINSIC PATHAY)
what should you INR be if you’re taking warfarin
2-3
what does a prolonged PT mean with normal PTT
liver disease, vitamin K insufiecnecy, defective clouting factors or WARFARIN
what does normal pt with prolonged put mean
defect clot factors, lupus anticoag, von will, autoimmune
what does prolonged PT & PTT-INR mean
defective factors, severe liver disease, warfarin over dose
what does D-Dimer test
rule out clotting (thrombotic episodes) (DVT, PE)
D-Dimer is one of the protein fragments produced when a blood clot gets dissolved in the body -> usually undetected
when is D-Dimer ordered
DVT symptoms (leg pain, edema, discolour) PE symtoms (SOB, cough, chest pain, rapid HR)
what does a negative D-Dimer test mean
person doesn’t have acute clot formation of breakdown
what does a positive D-Dimer mean
abnormally high fibrin degradation products, doesn’t tell us location or cause
elevated levels also after Sx, trauma, infection, MI, cancer or liver disease
*used to rule out, not confirm diagnosis
what is you HgB A1C if you don’t have diabetes vs. if you do
No diabetes <5.7%
Diabetes 6.5% or higher
what are the signs of hyperglycemia
increased thirst, frequent urination, blurry vision, slow healing
what are the signs of hypoglycaemia
sweat, hunger, tremble, anxiety, confusion, blurred vision
what id normal FBG
3.9-5.5
what is normal OGTT after 2 hr
<7.8 = norm
what are normal BG numbers
fasting: 4-7
Post-prandial (2 hr after meal): 5-10
random: <7
what does the oral glucose tolerance test determine
measures bodes ability to use glucose
what is the normal results of OGTT
fast: <7
1 Hr: <10.2
2 hr <7.7
what are the prediabetic response for OGTT
2 hr: 7.8-11.0
normal vs prediabetic vs diabetic HbA1C
Normal = <6 pre = 6.0-6.4 dia= 6.5+
what are the neurogenic/autonomic hypoglycaemia symptoms
Tremble, hunger, palpitations, nausea, sweating, tingle, anxiety
what are the neurglycopenic symptoms of hypoglycaemia
difficulty concentration ,vision changes, difficulty speaking, confusion, headache, weak, dizzy, drowsy, tired
what is mild-mod hypoglycemia
2.8-3.9mmol/L with autonomic symptoms
what do you do with mild-mod hypoglycaemia
1) 16g glucose or 4 tabs
2) repeat BG in 15 minutes
3) repeat until BG >4.0
4) give meal or snack
5) inform physician if happens 3+ times
6) document
what is severe-conscious hypoglycaemia
autonomic & neuroglycopenic symptoms & <2.8mmol
what do you do with severe conscious
1) 20g carbs
2) bg again 15 mins repeat until >4.0
3) meal or snack
4) physician
5) document
what is severe uncontious
same as severe continous except they not conscious
what do you do in severe uncontious
1) IV glucose, 25g as 50ml D50W over 1-3 minutes or 1mg glycogen SC
2) 10 min retest (redo step one title <4)
(max one glycogen shot)
3) ASAP inform doctor
4)Document
explain morphine
Reduces pain
opiod analgesic
side effects are Resp depress & conspitation
mechanism is it binds to opiod receptors in cans, alters perception & response to painful stimuli with generalized CNS depression
Assess: rr, bp, pain, narcan is less than 8 is less than 12 hold, urinary retention, cranial pressure, tolerance & physical dependence
what class of drug is lipitor / atorvastatin
lip lowering agent -> HMG-CoA reductase inhibitors
what is the indication for a atorvastatin
hypercholestemia. Prevent CAD. Lower LDL (2 weeks) must be taken life long
increases HDL & decreases Tg
what are the non lipid benefits of atorvastatin/lipitor
stability of atherosclerotic plaques decreases inflamation slows calcification improves abnormal endothelial function increases dilation decreases AFIB suppreses thrombin
what are the worst outcome for atorvastatin
LIVER DISFUNCTION CAN OCCUR (LFT tests prior & 3 months post) (ALT, AST)
Muscle pain, tenderness or weakness -> CHECK CPK (INDICATES MUSCLE INJURY)
n/v, heart burn, cramping, diarrhea, memory loss
can cause overweight fetus
CANNOT BE GIVEN WITTH LIVER DISEASE
what is the mechanism of atorvastatin action
increased LDL receptors on hepatocytes
inhibits HMG cos-reductase (rate limiting enzyme in cholesterol biosynthesis) = hepatocytes better able to remove LDLS
what is the therapeutic use of atorvastatin
hypercholesterolemia prevent CV primary prevention with normal LDD post MI therapy diabetes influenza
what class is metoprolol
beta blockers (Anti-anginas & anti-HTN)
what is the mechanism of metoprolol
blocks beta 1 receptors ( myocardial) adrenergic receptors (doesn’t usually affect beta 2)
what is the indication for metoprolol
HTN, angina, prevent MI . decrease mortality, management of HF
Unlabled for: ventricular arrhythmia, tremor, anxiety & migraine
what does metoprolol do?
blocks action of NE & E so it decreases HR & BP
what are the adverse effects of metoprolol
low bp, low hr, pulmonary edema, HF
when is metoprolol contraindicated
decreased hr or bp, pulmonary edema, heart block, cariogenic shock, signs of HF
CANT GIVE WHEN BPM UNDER 50
teaching about metoprolol
abrupt withdrawal can lead to arrhythmia, HTN, ischemia
may cause drowsiness & orthostatic HTN
when is hydrochlorthizide in effective
with a low GFR
what class is hydrochlorothiazide
antiHTN, thiazide diuretics
when is hydrochlorothiazide indicated
HTN, edema
what is hydrochlorothiazide mechanism
increased urine production via block or reabsorption of Na+ & chloride in early DCT (smaller amt than loop)
Dependent on kidney function - INEFFECTIVE WITH A LOW GFR 15-20
Diuresis within 2 hours, 4-6 hr peak, duration 10 hour
what are the adverse effects of hydrochlorothiazide
hyponatremia, hypochloremia, dehydration, hypokalemia
hyper uricemia
increased LDL
increased excreted MG
what kind of drug is furosemide
loop diuretic
what is the mechanism of furosemide
acts on henley loop to block reab or Na & CL-
prevent passive reabsorption of H20
oral onset is 60 minutes for 8 hours
IV onset is 5 min for 2 hours
what are indications for furosemide
pulmonary edema, edema, HTN
what are the adverse effects of furosemide
hyponatremia hypochloremia dehydration hypotension hypokalemia ototoxicity hyperglycaemia hyperuricemia reduces LDL, raises HDL NOT SAFE FOR PREG
what type of insulin is lispro/humalog
RAPID ACTING ANALOG of regular insulin
when would lispro/humalog be given
food must be in front of them -> immediately b4 meals
what is the onset of lispro/humalog
10-15 minutes
what is the peak of lispro/humalog
60-90 minutes
what is the duration of lispro/humalog
3-5 hr
what is the color of lispro/humalog
clear
can you mix lispro/humalog
yes with NPH
why does lispro/humalog work faster than regular
aggregates less than normal insulin b/c of a changed animo acid so is absorbed pasted
usually SC
what type of insulin is glargine/lantus
long acting basal insulin analogue
what is the onset of glargine/lantus
90 mins
what is the peak of glargine/lantus
non
what is the duration of glargine/lantus
24 hours
what are some special considerations of glargine/lantus
DO NOT GIVE IV DO NOT MIX WITH OTHER INSULIN DOSING CAN OCCUR AT ANY TIME LOW SOLUBILITY SO EXTENDED RELEASE is clear
what is warfarin
vitamin K antagonist
what does warfarin do
prevents thrombosis
delayed onset -> inappropriate for emergencies
LT prophylaxis
poses a huge hermorage risk
what is the mechanism of warfarin
decreased clotting factor production (by inhibiting enzyme needed to convert vitamin K to active form)
* no effect on clotting factors already in circulation
when does warfarin start to work
Onset: 8-12 hours
peak: 72-96 hours
Direction 2-5 days
what is the therapeutic use of warfarin
prevent VT
prevent PE, thromboembolism with prosthetic valve, thrombosis from AFIB, decreases TIA & MI risk
what do u need to monitor for warfarin
PT-INR 2-3 for most
daily for first 5 days
what are side effects of warfarin
hemorrhage, skin necrosis, weak bones, fever, GI disturb
when is warfarin contraindicated
thrombocytopenia. Lumbar puncture. Recent CNS surgery. Hi risk bleeders (Hemophilia, aneurysm, GI ulcer, HTN, abortion)
vitamin K deficiency, Liver disease, alchoholism
pregnancy & lactation
*KEEP VIT K INTAKE STABLE
what kind of drug is ramipril
Ace inhibitor
what does ramipril do
lowers bp b/c not angio 2 which causes there to be vasodilation & decreased heart workload
what are the indications for ramipril
treats HTN, HF, MI (prevent)
what are the side effects of ramipril
hypotension, Increasd K, cough, kidneys disease need reduced dosage, fetal death
what do assess for ramipril
Bp (HR not most important) electrolytes, K+, dry cough
what is digoxin
Cardiac glycoside - effects both mechanical & electrical
what does if the effect of digoxin
increases myocardial contractility & effects on neural hormonal
CAN CAUSE DANGEROUS DYSRYTHMIAS EVEN WITHIN THERAPEUTIC DOAGE
DOESNT PROLONG LIFE - SYMPTOM RELIEF ONLY. Increases exercise tolerance & decreases hospital stay
what are the indications for digoxin
HF, dysrhythmias
what is mechanism of digoxin
IT IS A POSITIVE INOTROPE -> increases the force of ventricular contraction -> increased CO
- Inhibits na+/K+ATPASE -> which promotes Calcium accumulation in the myocytes ->augments contractile force
- K+ IONS COMPETE TO BIND Na+/K+ATPASE so when K+ is low, excessive inhibition occurs -> toxicity
- K+ MUST BE MONITORED
what are the benefits of digoxin
increased CO
Decreased sympathetic tone. increased urine, decreased renin, decreased heart size & fatigue reduced.
what are the side effects of digoxin
Dysrythmias b/c hypokalemia or OD (0.5-0.8 ideal)
anorexia, N/v, fatigue, visual distrubance,
when do hold Digoxin
if HR <60
what class is hydralazine
direct action vasodilator
what is the effect of hydralazine
direct relaxation of arteriolar smooth muscle
(no effect on veins)
(BP falls)
(HR & myocardial contraction increases)
what is onset & duration for hydralazine
PO 45 minutes for 6 hr
IV: 10 minutes for 2-4 hours
what is the therpeatuic use for Hydralazine
essential HTN with a beta blocker
HTN crisis ( 220/130)
HF
what are the side effects of hydralazine
reflex tachycardia, increased blood volume, systemic lupus erythmatosis
what should you monitor for HYDRALAZINE
BP, ECG, O2, RR.
hold if BP LOW
