Studied by 30 PeopleThe mother of a very fussy and colicky one-year-old notices that her child’s black T-shirt is crusted over with dried salt after being outside on an extremely warm day. What (inborn) disorder could this be a sign of? What labs to order?
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The mother of a very fussy and colicky one-year-old notices that her child’s black T-shirt is crusted over with dried salt after being outside on an extremely warm day. What (inborn) disorder could this be a sign of? What labs to order?
Cystic fibrosis Sweat Chloride testing – Cystic fibrosis mutations
A 27 year old trainer in a local gym experiences acute and worsening chest pain. His labs come back with a total creatine kinase (CK) activity that is four-fold elevated as compared with the normal upper limit of the reference range. What additional labs would be informative in this setting?
CK-MM (muscles)
CK-MB (heart)
CK-BB (brain)
Caused by strenuous exercises – CK testing of the blood
Given pCO2 and HCO3, calculate and interpret pH levels using the Henderson-Hasselbalch buffer equation
PH calculation given pCO2 and HCO3
PH = 6.1 + log (HCO3)/(H2CO3)
PH = 6.1 + log (HCO3)/ (0.03 x pCO2)
H2CO3 = 0.03 x pCO2
expected ABG results (pCO2, pO2, HCO3-, pH) and potassium values for the following: Metabolic Acidosis
Metabolic acidosis: pH <7.35, low PCO2 (<36), low HCO3 (<21), K level high
expected ABG results (pCO2, pO2, HCO3-, pH) and potassium values for the following: Metabolic Alkalosis
Metabolic alkalosis: pH >7.45, high PCO2 (>44), high HCO3 (>27), K level low
For the following acid-base imbalances, list expected ABG results (pCO2, pO2, HCO3-, pH) and potassium values for the following: Respiratory Acidosis
Respiratory acidosis: pH < 7.35, high PCO2 (>44), high HCO3 (>27)
For the following acid-base imbalances, list expected ABG results (pCO2, pO2, HCO3-, pH) and potassium values for the following: Respiratory Alkalosis
Respiratory alkalosis: pH > 7.45, low PCO2 (<36), low HCO3 (<21)
anion gap equation
Na – CL + HCO3
high anion gap?
metabolic acidosis
Explain what compensatory mechanisms arise in the context of Metabolic Acidosis
Metabolic acidosis: respiratory alkalosis increased respiratory rate to decrease PCO2; Kussmaul breathing) – associated with hyperkalemia
Explain what compensatory mechanisms arise in the context of Metabolic Alkalosis
Metabolic alkalosis: respiratory acidosis (slow breathing) (renal and respiratory) – associated with hypokalemia
Explain what compensatory mechanisms arise in the context of: Respiratory Acidosis
Respiratory acidosis: metabolic alkalosis (renal – slow bicarbonate reclamation) – COPD, overdose
Explain what compensatory mechanisms arise in the context of: Respiratory Alkalosis
Respiratory alkalosis: metabolic acidosis (dumping of bicarb) – caused by hyperventilation
List factors that shift the oxyhemoglobin dissociation curve to the right and the consequences in regard to oxygen delivery to the periphery
Low pH, decreased O2 affinity (T state), increased oxygen delivery (low pH, increased CO2, high temp, high 2,3-BPG, low O2 affinity hemoglobin variants)
List factors that shift the oxyhemoglobin dissociation curve to the left and the consequences in regard to oxygen delivery to the periphery
High PH, increased O2 affinity (R state), decreased oxygen delivery (high pH, decreased CO2, low temp, low 2,3-BPG, high O2 affinity Hemoglobin variant, fetal hemoglobin (HB F))
Identify the p50 in mmHg from inspection of an oxyhemoglobin dissociation curve
P50 is the partial pressure of oxygen that causes hemoglobin to be 50% saturated
50% of Hemoglobin saturation determines the P50 partial pressure (mmHg)
Explain how HCO3 works as a volatile buffer
HCO3 takes up protons from HB and becomes carbonic acid In the lungs carbonic acid (H2CO3) is converted to CO2 and water by carbonic anhydrase
Describe how the kidney handles acid or base excess using ammonia, carbonic anhydrase, the anion exchanger (HCO3/Cl), the H+ ATPase and the Na+/H+ and K/H+ exchanger
Proximal tubule: 70-80% of HCO3 recycling – HCO3 reabsorption – secondary active transport Distal tubule: 20-30% of HCO3 recycling – H+ secretion Respiratory alkalosis– low PCO2 causes high pH which causes low HCO3 reabsorption and low H + secretion – causing compensation
Respiratory acidosis – high PCO2 causes low PH and compensate by high HCO3 reabsorbing and high H+ secretion
Metabolic acidosis – if H+ high and HCO3 low causes kidney to compensate by increasing H+ secretion and increasing HCO3 absorption
Metabolic alkalosis – if H+ low and HCO3 high causes kidney to compensate by decreasing H+ secretion and decreasing HCO3 reabsorption
How does an oximeter work and what does it measure?
Uses absorbance Maxima of Hb derivatives and differential equations to quantify (%): Oxyhemoglobin, Deoxyhemoglobin, carboxyhemoglobin (CO-Hb), Methemoglobin (Fe-Hb)
spectrophotometry (Hb variants change color of blood)
Explain why lactate is the final end product of anaerobic glycolysis
So by converting pyruvate to lactate, that is a reduction that requires NADH, cytosolic NADH, and therefore liberates NAD to really participate in the glyceraldehyde-3 phosphates step. So it's a way of keeping anaerobic glycolysis going in the cytoplasm of the muscle and rbc.
monosaccharides
pentose (5 carbons – ribose), hexoses (6 carbon – glucose, fructose, galactose)
disaccharides
sucrose, lactose, maltose
glycogen
one form in which body fuel is stored; stored primarily in the liver and broken down into glucose when needed by the body
acetoacetate
B-hydroxybutyrate
lactate
Identify biological activities of insulin
-secreted by pancreatic beta cells -Inhibits glucagon -Induces glucokinase -Increases transport of glucose into liver, skeletal muscle, and adipose tissue
Identify biological activities of Glucagon
-secreted by pancreatic alpha cells in islet (a response to decreasing plasma glucose) -quickly raises blood sugar and inhibits insulin secretion. -signals carbohydrate starvation causes the liver to export glucose -Inhibits glycolysis and uptake of glucose by liver -Stimulates gluconeogenesis, glycogenolysis and mobilization of fatty acids from adipose cells Medication for people with hypoglycemia
Identify biological activities of cortisol
adrenal steroid hormone – high levels promote gluconeogenesis – starvation state hormone – favored by untreated diabetes mellitus.
Identify biological activities of GLP-1 (Glucagon-like peptide-1
inhibits glucagon release from alpha cells in pancreatic islets. GLP-1 analogs used for treatment in type 2 diabetes
Identify biological activities of GIP (Gastric inhibitory peptide)
glucose-dependent insulinotropic polypeptide. GIP analogs used for type 2 diabetes
Identify biological activities of DPP-4 (dipeptidyl peptidase-4):
rapidly degrades GLP-1 and GIP. DPP-4 inhibitors use for treatment of type 2 diabetes.
Boost insulin secretion in individuals with type 2 diabetes
Type 1 DM
immune mediated diabetes. Pancreatic beta cell destruction (immune destruction of pancreas) (B and T cell mediated). Autoantibodies against stuff in islet cells. Get insulin replacement.
Type 2 DM
insulin resistance and impairment of insulin secretion
Gestational DM
transient effect of placental hormones
MODY
rare autosomal dominant mutations in hepatic nuclear factors (HNF14, HNF4A) and glucokinase
Identify risk factors for type 2 DM and long term complications
-geographical, ethnicity, body mass index, inactivity, obesity. Nicotine (smoking) is a direct vascular toxin for coronary vascular disease which is a component of diabetes -Long-term complications: retinopathy, nephropathy, and coronary vascular disease
long term complications of type 1
etinopathy, nephropathy, and coronary vascular disease
Hemoglobin A1c screening is performed to screen for type 2 diabetes but not for type 1. Why?
A1C reflects average blood glucose value in the last 2-3 months. Useful in diagnosing diabetes and monitoring long-term efficacy of glucose control.
There is low sensitivity for type 1 diabetes.
Interpret HA1c % in the context of non-diabetic individuals, and those with pre-diabetes and diabetes mellitus
Contrast HA1c and fructosamine in regard to the time period of glucose control they reflect
-HA1C: A1C reflects average blood glucose value in the last 2-3 months -Fructose amino only over the last few weeks because of the circulating half-life of red cells and albumin
Identify HA1c measurement techniques and common interferences
Measurement techniques: column chromatography method, electrophoresis, high pressure liquid chromatography (HPLC), immunoassay and more.
Common interferences: hemoglobin variants like Hemoglobin S and hemoglobin C. Hemolytic anemia (short half-life or life span of RBCs – sickle cells – 14 days in HBS).
common autoantibodies included in working up individuals with type 1 diabetes
islet cell antibodies, glutamic acid decarboxylase (GAD-65), insulin autoantibodies (IAA), and IA-2A, and protein tyrosine phosphate
List ADA guidelines for the diagnosis of type1
Fasting Plasma glucose >126mg/dL (7.0mmol/L), 2-H Plasma Glucose >200 mg/dL, Plasma blood glucose recommended for acute onset of type 1 in individuals with symptoms of hyperglycemia (random plasma glucose >200 mg/dL (11.1 mmol/L)).
List ADA guidelines for the diagnosis of type 2
FPG >126 mg/dL. 2-H PG >200mg/dL, A1C >6.5%, patients with hyperglycemia – random plasma glucose >200 mg/dL
List ADA guidelines for the diagnosis of pre-diabetes
BMI, overweight – A1C >5.7 %, FPG >126 mg/dL. 2-H PG >200mg/dL
List ADA guidelines for the diagnosis of gestational DM
when oral glucose tolerance testing with plasma glucose measurement fasting (92 mg/dl), 1 hr into fasting (180 mg/dl), 2 hr into (153 mg/dL).
If plasma glucose level 1 hr after non-fasting >130 mg/dL and more.
What are the expected values for glucose, pH, bicarbonate, sodium, potassium and pCO2 in the setting of diabetic ketoacidosis?
Glucose: hyperglycemia – high glucose
PH: low
Bicarbonate: low
PCO2: low (compensation)
Sodium: low (hyponatremia)
Potassium: high (hyperkalemia) – cells take H+ and exchange for potassium
