Week 4- Lecture 3 - Clinical Models Flashcards
cirrhosis clinical manifestations
severity related
- ascites can be described based on volume of fluid in the peritoneum
- moderate to large volume
- 500ml is detectable by US
- 1500ml is detectable by clinical examination
moderate to severe abdominal discomfort
increased weight severe sodium retention
dilution hyponatremia (due to water retention)
renal failure
Cirrhosis diagnostic criteria
history and P/E
changes in body weight
abdominal girth/circumference measurement
liver, renal and cardiac function : determine systemic damage/dysfunction
laboratory analysis
- ascitic fluid analysis
1. serum - acetic albumin gradient (SAAG)
>1.1g/dL : portal hypertension or transudative ascites
<1.1g/dL : exudative ascites
2. amylase cc . increase pancreatic origin
3. WBC increase : infection
4. RBC increase : malignancy / hemorrhage
Cirrhosis treatment
volume is the primary determinant of treatment
diuretics
- promote ascitic fluid loss
- normalise sodium balance
severe cases : paracentesis
- insertion of cannula into peritoneal cavity to remove ascitic fluid
- after paracentesis : intravenous albumin if large amount of fluid is removed
- prevent circulatory dysfunction and rapid reoccurrence of ascites
Dehydration clinical manifestations
decreased level of consciousness
prolonged capillary
dry mucous membranes
decreased or absent tears
change in vital signs
- increased RR
- decreased BP
- weak pulse
depressed fontanel
decreased (oliguria) or absent (anuria) urine output
Diagnostic criteria dehydration
history and P/E
- loss of skin elasticity (turgor)
- fluid intake (volume and type : hypertonic/hypotonic)
- fluid output quantity and type (urine/stool/emesis/sweat)
Severe cases : laboratory analysis
- blood concentrations of electrolytes (sodium, potassium, Cl) and bicarbonate (acid-base balance) (anion gap)
poor perfusion may lead to renal damage, build up of lactic acid (metabolic acidosis)
- blood urea nitrogen (BUN level increase due to impaired excretion)
-creatinine (serum creatinine increase due to renal blood flow)
-specific gravity - urine osmolality is indication of kidney ability to excrete /conserve water
concentrated urine : more particles - higher specific gravity
diluted urine : lower concentration of particles - lower specific gravity
treatment plan formulation based on data
Dehydration treatment
- rehydration
- correction of electrolyte balance
mild to moderate : oral administraiton
- fluids contain: sodium potassium, glucose
-appropriate proportion to promote ready absorption from GI tract to circulation
-frequent administration, small amounts
Severe : intravenous administration
- ringer’s lactate or isotonic saline
-restore plasma concentrations
- large volume fluid replacement
volume replacement amount should be based on fluid deficit amount
- avoid rapid correction of hyponatremia :associated with neurologic complications
- avoid rapid corruption of hypernatremia : cellular swelling, cell rupture
Highly Active Antiretrovial Therapy (HAART) associated acidosis clinical manifestations
symptoms are related to the severity of metabolic acidois
- most individuals with hyperlactatemia : asymptomatic
- mild hyperlactatemia
- nausea
- vomiting
- abdominal discomfort
- weight loss
- hepatic steatosis (fatty liver) fat deposition
severe hyperlactatemia
- metabolic acidosis : lactic acidosis syndrome (LAS) - pH <3
- liver enlargement (hepatomegaly), elevated liver enzymes, hepatic failure
- coma, multiple organ failure
Diagnostic criteria (HAART)
early recognition and treatment of hyperlactatemia to decrease morbidity and mortality
history of NRTI use
laboratory diagnosis
- blood lactate levels
- blood pH, electrolyte levels
- liver function tests to see hepatic dysfunction
treatment HAART
drug selection may influence the development of hyperlactatemia
- certain drugs deplete mitochondrial DNA more than others
treatment is determined by symptoms
- subclinical hyperlactatemia : no treamtne
-if symptoms develop but not lactic acidosis yet
- alternate selection of NRTI combinations
- if symptoms develop with lactic acidosis :
interruption with NRTI treatment, but recovery cannot be assured
intravenous fluid administration to :
- expand intravascular volume
- prevent cardiovascular collapse
- promote renal clearance of lactate
weeks may be needed to recover
resolution is confirmed by
- normal sodium bicarbonate, normal pH, normal liver function, normal lactate levels
Renal tubulopathy clinical manifestations
HPS hyperprostagladnin E syndrome (antenatal bartter syndrome) : pregnancy /inutero
- neonates have severe effects
- maternal hydraminos (excessive amniotic fluid)
- increased detail urine output
Bartter syndrome and Gitelman syndrome present early infancy, childhood and adolescence
- increased urine output (polyuria)
- Hypercalciuria (excessive calcium urine)
- effects from excessive prostaglandin
- fever (effect on hypothalamus) , vomiting, diarrhoea (effect on fluid/electrolyte movement into the intestine, increased secretion) – worsens fluid and electrolyte imbalance
growth retardation
cardiac arrhythmia and sudden death
- may result from electrolyte imbalances
failure to thrive and developmental delay
- common in untreated patients
significant decrease in bone mineral density
diagnostic criteria Renal Tubulopathy
in families with know risk : genetic testing
- amnionic fluid or cell sample after birth
renal structures by US
laboratory studies
- urine and serum electrolyte studies
-arterial blood gases (ABGs)
Anion gap
base excess
urine specific gravity to determine fluid balance
renal tubulopathy treatment
correction of
- renal salt loss (hyponatremia, hypokalaemia)
- fluid loss
pharmacologic - sodium and potassium supplements - potassium sparing diuretics -calcium and magnesium supplementations protaglandin inhibitors
