clw 7 Flashcards
UTI, diabetes, palliative care, ckd
is GGT specific to liver issues?
no. GGT is found also in the kidney and pancreas besides the liver.
Non-hepatic causes of increased GGT include: pancreatic disease, MI, renal failure, alcoholism, certain medications, COPD
what does hazy appearance of urine point to
possible presence of proteins, cells, casts
what is specific gravity of urine
A urine-specific gravity test compares the density of urine with the density of water. The test may help healthcare professionals identify dehydration, a kidney problem, or a condition like diabetes insipidus
pyuria hints at
UTI
A & O
alert and oriented
what does high urea and scr point to
dehydration / kidney problems
pyelonephritis symptoms
WBC cast present, fever, rigours, headache, nausea, vomiting, and malaise, flank pain, costovertebral tenderness (renal punch), or abdominal pain
cystitis symptoms
dysuria, urgency, frequency, nocturia, suprapubic heaviness or pain; gross hematuria
remember that elderly without fever does not mean no infection/sickness! watch out for?
delirium, confusion, urinary incontinence, loss of appetite
healthcare associated/nosocomial pyelo
- Nosocomial – onset of UTI >48h post admission
- Healthcare associated - patients who have been hospitalized or
underwent invasive urological procedures in the last 6 months,
has an indwelling urine catheter, etc
risk factors for uti
Female, Dehydration, Diabetes, presence of glucose in urine, Elderly
abx in uti
cephalexin, cotrimoxazole, augmentin, cipro
nitrofurantoin,fosfomycin (only cystitis)
abx for poor renal fx uti
cephalexin, augmentin, cipro
does amox clav cover MDR organisms? often found in nursing homes
amoxclav does not cover. fosfomycin preferred
abx for uti for pregnancy
fosfomycin, amoxclav
benefit of fosfomycin over other abx
one time dosing, improve patient adherence
abx of high resistance in sg
cipro, cotrimoxazole
aminoglycosides avoid in
kidney toxicity, otoxicity
need repeat culture for uti if positive response to tx?
no
GOT of uti
resolution of symptoms by 24-72h
when making a recommendation for drug therapy, what else to monitor besides improvement of sx?
list down side effects of drug therapy recommended
UTI non pharm
- Rehydrate the patient (supervised hydration for pts with heart failure)
- Scheduled voiding
- Wear loose-fitting clothes and cotton underwear
- After using the toilet, wipe from front to back (especially after a bowel movement). Keep genital area dry
- time voiding
if pt has extensive comorbidities and hypoglycemic ep, and old age, treatment goal hba1c?
<8.0%
what happens if patient takes medicine for diabetes without eating? (eg. sulfonylureas)
hypogly ep!
glibenclamide pk
long acting SU with ACTIVE metabolites, can accumulate and cause hypogly
why avoid SUs with long t half
can accumulate in body and cause hypogly
when going thru an episode of hypogly in the hospital, how to reduce meds
Using both insulin glargine (basal insulin) and sulfonylurea → should either discontinue the sulfonylurea or decrease the dose by 50%
GOT of hypogly
- Normalise blood glucose levels
- Prevent future occurrence of hypoglycemia
how to tackle an episode of hypogly
15-15-15 → 15g of fast acting sugar every 15 minutes
diabetes what to TCU
Foot and eye exam, renal function, BP at every visit
hba1c q3m
metformin what to look out for
metabolic acidosis
what is the triple whammy causing AKI
combined use of diuretics, RAASi and NSAIDs
aspirin is only for primary prevention for stroke/ami. who qualifies?
<70 yo (bleeding risk vs prevention of stroke)
GOT of palliative care
meet nutritional needs,
keep patient comfortable
diuretic must stop if
dehydrated, AKI
end of life, how to monitor blood sugar
manage episodes symptomatically, do not need to track hba1c
insulin heavily bound to albumin
yes, extensive
rapid acting insulin
lispro, aspart, glulisine
short acting insulin
regular
intermediate acting insulin
nph
long acting insulin
detemir, glargine
how does ckd affect drug absorption
- Decreased gastric acidity e.g. due to urea retention
- Drug interactions e.g. with phosphate binders, antacids and vitamin supplements
how does diabetes affect drug absorption
Delayed gastric emptying e.g. due to
gastroparesis
how does ckd affect drug distribution
fluid imbalances affecting volume of distribution, hydrophilic drugs will be affected , where by Vd will increase due to the extra water in the body
how does ckd affect drug metabolism
Accumulation of metabolites: Especially if route of elimination
of metabolite is via glomerular
filtration
how is albumin affected in ckd
Albumin is decr in CKD → incr free drug fraction for drugs that are highly-bound to albumin → incr Vd of the drug
how are cyp enzymes affected in ckd
CKD can alter function of transporters and CYP enzymes in the gut due to uremic toxins → accumulation of active metabolites in the body
what is the sick day advice for sglt2i
when pt face acute illness assoc with nvd, causing decreased fluid intake, stop sglt2i temporarily
sglt2i se
genitourinary infections, diabetic ketoacidosis (vomiting, ab pain, SOB)
type 2 dm
Progressive loss of adequate β-cell insulin secretion on the background of insulin resistance
top 3 s/sx of dm
excessive hunger, thirst, peeing
GOT of diabetes
prevent microvascular (eg. neuropathy, retinopathy) and macrovascular (cardio) complications
non pharm of diabetes
- Quit smoking
- Weight Reduction (7% loss of IBW)
- Exercise (150 minutes of moderate activity, 2 days per week of muscle strengthening abv 55yo)
- Diet
- DIABETIC FOOT ED
avoid beta blockers with sulfonylureas
mask hypoglycemia
metabolism of sulfonyureas
cyp2c9
benefit of tzd
fatty liver disease
tzd cannot be used in
heart failure esp nyha 2/3
sglt2i c/i
dialysis, egfr<20
What to do with oral therapies when starting injectables
Metformin: No change
SGLT2i: No change
SU: (If basal insulin initiated) Discontinue or reduce dose by 50%; (if mealtime insulin initiated) discontinue SU
TZD: Discontinue or reduce dose
DPP4: Discontinue if GLP initiated
diabetic ketoacidosis sx
plasma glucose >13
urine ketone positive
anion gap >10 (acidosis)
alert
hyperglycemic hyperosmolar state type 2
plasma glucose >33
urine ketone neg
anion gap <12
coma
LDL goal for DM + risk factor, neuropathy etc or >10 y
<1.8mmol/l
LDL goal for DM < 10 y
<2.6mmol/l
when to treat TG in DM
> 4.5
UTI complicated cystitis objectives
- WBC >10 signifies pyuria
- RBC >5/HPF signifies hematuria
- Gram stain: bacterial or yeast infection
- Leukocyte esterase activity in urine
gout urate levels target
Urate level < 6 mg / dL
gout GOT
Rapid and effective pain relief
Reduce future attacks
Prevent joint destruction, tophi formation
when to start ULT
Start 2 to 3 weeks after acute attack
when starting ULT add what
Initiation needs anti-inflammatory prophylaxis for 3-6 months
Colchicine 0.5mg OD
signs of ckd
Fatigue, weakness, SOB, mental confusion,
N/V, bleeding, loss of appetite, itching, cold
intolerance, weight gain, neuropathy, uremic breath
labs of ckd increased
- SCr, urea, K, P, PTH, BP, glucose, lipids,
decreased labs in ckd
GFR, CrCl, CO2 (metabolic acidosis), Hgb (anemia), iron stores (Fe deficiency), 25(OH)D (vit
D deficiency), albumin (malnutrition), glucose, Ca
(early stages of CKD), HDL
raised levels of ckd, concern for hyper-?
K, Mg, P, uric acid
ckd GOT
- Slow down progression of disease and delay need
for renal replacement therapy (RRT) – dialysis or
transplantation - Maintain fluid and electrolyte homeostasis
- Provide adequate nutritional and metabolic support
- Prevent and treat extra-renal complications (anemia
and bone disease)
when can acei/arb be continued in aki
-Increase in SCr < 25-30% from baseline value
- Serum K≤ 5.5 mmol/L
diuretics used in CKD with HTn
thiazide / loop (esp if reduced crcl)
elimination of atenolol and bisoprolol
renal
for ckd patients, need statin?
yes, do not need monitoring. Increased risk for atherosclerosis, CVD and mortality (regardless
of LDL levels)
fibrates can use for ckd?
stage 1 to 3 only
fluid intake for ckd
1-1.5 L/day
salt restriction for ckd?
2g of Na aka one teaspn of salt
what painkiller to avoid in ckd
nsaid (risk for nephrotoxicity)
how do hydrophilic molecules like to travel by
Paracellular
Through the water-filled gap junctions between two cells, passive process via diffusion
how do lipophilic, uncharged and low MW (<300Da) molecules like to travel by
Transcellular
absorption directly through the lipid bilayer of cells,
passive process via diffusion (down a conc gradient so will diffuse from lumen of intestine to blood)
how do molecules in GIT travel by
In GIT, the paracellular route is v tight to prevent microorganisms frm food to get into the bloodstream easily → hence, via GIT, v little paracellular transport (most of the abspt occur via transcellular)
do glicazide and glipizide have active metabolites
no
what does high Vd tell us about the drug
Lphilic → distribute widely in tissues/conc somewhere else in the body → high V
what does small Vd tell us about the drug
Hphilic, charged→ stay in plasma (cannot pass through via transcellular route to the tissues)→ small V
enteric coating made up of
pH-sensitive polymers
purpose of enteric coating
protect patient
protect drug
ideal log p value for oral drug for good intestinal and oral absorption
log p<5, ideally 1.38-1.43b
PK parameter used to quantify drug absorption
F
(fraction of administered dose that reaches systemic circulation)
first line for esbl
carbapenem (imipenem)
