Short explanations Flashcards

(157 cards)

1
Q

What is Creatinine?

A

A waste product generated from muscle metabolism, filtered by the kidneys to assess renal function.

Creatinine is derived from the breakdown of creatine phosphate.

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2
Q

What does elevated CRP (C-Reactive Protein) levels indicate?

A

Inflammation or infection, used to monitor disease activity in various conditions.

Conditions include infections, autoimmune diseases, and cardiovascular risk.

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3
Q

What role does Bicarbonate (HCO₃⁻) play in the body?

A

Maintains acid-base balance as a component of the blood buffering system.

Low levels suggest metabolic acidosis; high levels may indicate metabolic alkalosis.

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4
Q

What is Hypergammaglobulinaemia?

A

An increase in gamma globulin levels in the blood, often due to chronic inflammation, infection, or plasma cell disorders.

Examples include multiple myeloma or chronic liver disease.

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5
Q

What can the measurement of enzymes in plasma indicate?

A

Biomarkers for organ damage.

Examples include ALT/AST for liver injury, CK-MB/Troponin for cardiac injury, and Amylase/lipase for pancreatic disorders.

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6
Q

What does urinary volume measurement help evaluate?

A

Kidney function, fluid balance, and endocrine disorders.

Abnormal volumes can indicate conditions like renal failure or diabetes insipidus.

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7
Q

What is LDL - Cholesterol commonly referred to as?

A

Bad cholesterol, as high levels contribute to atherosclerosis and cardiovascular disease.

LDL carries cholesterol to tissues and is a target for lipid-lowering therapy.

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8
Q

What is the purpose of corrected calcium measurement?

A

Accounts for serum albumin levels when interpreting calcium concentration.

Corrected Ca = Measured Ca + 0.02 × (40 - Albumin) (g/L).

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9
Q

What are Apolipoproteins?

A

Proteins that bind lipids to form lipoproteins, involved in lipid transport and metabolism.

Key examples include ApoA-I (associated with HDL) and ApoB (associated with LDL).

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10
Q

Define Isoenzymes.

A

Different molecular forms of an enzyme that catalyze the same reaction but differ in structure and tissue distribution.

Examples include CK-MB (heart) and CK-MM (muscle).

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11
Q

What is urate?

A

Urate (or uric acid) is the end-product of purine metabolism.

Elevated levels can lead to gout or renal stones. Measured to assess gout, kidney function, or tumor lysis syndrome.

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12
Q

What is alpha 1-antitrypsin?

A

A serine protease inhibitor that protects tissues from enzymes of inflammatory cells.

Deficiency can lead to early-onset emphysema and liver disease.

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13
Q

What does LDL stand for and what is its role?

A

Low-Density Lipoprotein carries cholesterol from the liver to peripheral tissues.

Often called “bad cholesterol” due to its role in plaque formation and cardiovascular disease.

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14
Q

What is transferrin?

A

An iron-binding glycoprotein that transports iron in the blood.

Used to assess iron status. Elevated in iron deficiency, decreased in chronic disease or malnutrition.

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15
Q

What is creatinine kinase (CK or CPK)?

A

An enzyme found in muscle, brain, and heart.

Elevated in muscle damage, myocardial infarction, and rhabdomyolysis. CK isoenzymes (CK-MB) help localize tissue injury.

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16
Q

What is gestational diabetes?

A

A form of glucose intolerance diagnosed during pregnancy.

Increases the risk of complications for both mother and baby. Diagnosed via oral glucose tolerance test (OGTT).

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17
Q

What are natriuretic peptides?

A

Hormones released from the heart in response to ventricular stretch and volume overload.

BNP and NT-proBNP are used in the diagnosis and monitoring of heart failure.

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18
Q

What is gamma-glutamyl transferase (GGT)?

A

A liver enzyme involved in glutathione metabolism.

Elevated in cholestasis, alcohol use, and hepatic enzyme induction. Often used to confirm hepatic origin of raised ALP.

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19
Q

What is the coefficient of variation (CV)?

A

A measure of relative variability calculated as CV = (Standard Deviation / Mean) × 100.

Used in lab quality control to assess precision of assays — lower CV indicates better precision.

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20
Q

What is troponin?

A

A cardiac-specific protein released into blood following myocardial injury.

High-sensitivity troponin assays are the gold standard for diagnosing acute myocardial infarction.

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21
Q

Fill in the blank: Elevated levels of urate can lead to _______.

A

gout or renal stones

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22
Q

True or False: Alpha 1-antitrypsin deficiency can lead to early-onset emphysema.

A

True

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23
Q

Fill in the blank: LDL is often referred to as _______.

A

bad cholesterol

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24
Q

True or False: Transferrin is decreased in iron deficiency.

A

False

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25
What role does creatinine kinase (CK) play in muscle injury?
Elevated in muscle damage, myocardial infarction, and rhabdomyolysis.
26
What is Therapeutic Drug Monitoring (TDM)?
Measurement of drug concentrations in blood to maintain a therapeutic range ## Footnote Used for drugs with a narrow therapeutic index, e.g., digoxin, lithium, anticonvulsants.
27
What are apolipoproteins?
Proteins that bind lipids to form lipoproteins ## Footnote ApoA-I is associated with HDL (protective) and ApoB is associated with LDL (atherogenic). Used in cardiovascular risk assessment.
28
What does creatinine clearance estimate?
Glomerular filtration rate (GFR) using serum and urine creatinine ## Footnote Reflects kidney function and is reduced in chronic kidney disease.
29
Define Chronic Kidney Disease (CKD).
Progressive decline in kidney function over time ## Footnote Staged by eGFR and albuminuria, with lab findings including elevated urea, creatinine, and electrolyte imbalances.
30
What is hepatitis?
Inflammation of the liver, commonly due to viral infection ## Footnote Lab diagnosis involves ALT/AST elevation, bilirubin, and serological markers.
31
What is bilirubin?
A breakdown product of haemoglobin ## Footnote Unconjugated bilirubin is elevated in haemolysis, while conjugated is elevated in liver disease or bile duct obstruction.
32
What are control intervals used for?
Assessing if lab results are within acceptable variation ## Footnote Also called control limits, part of internal quality control (IQC).
33
How is the Coefficient of Variation (CV) calculated?
CV = (SD / Mean) × 100 ## Footnote A measure of assay precision; lower CV indicates better reproducibility.
34
What is gestational diabetes?
Glucose intolerance first detected during pregnancy ## Footnote Diagnosed via oral glucose tolerance test (OGTT) and increases risk for both mother and fetus.
35
What do aminotransferases (AST & ALT) indicate?
Hepatocellular injury ## Footnote ALT is more liver-specific while AST is also found in muscle, markedly elevated in acute hepatitis.
36
What does osmolality measure?
Solute concentration in plasma or urine ## Footnote Used in evaluating hyponatraemia, SIADH, and dehydration.
37
What is pseudohyponatraemia?
False low sodium reading due to hyperlipidaemia or hyperproteinaemia ## Footnote Occurs when using indirect ion-selective electrodes.
38
What are enzyme assays?
Tests measuring the activity or concentration of enzymes in blood ## Footnote Used to diagnose tissue damage (e.g., CK, ALT, LDH) or inborn errors of metabolism.
39
Define diagnostic sensitivity.
Ability of a test to correctly identify patients with the disease ## Footnote Used to evaluate the diagnostic performance of tests.
40
Define diagnostic specificity.
Ability of a test to correctly identify patients without the disease ## Footnote Used to evaluate the diagnostic performance of tests.
41
What are reference ranges?
The expected range of values in a healthy population ## Footnote Depends on age, sex, method used, and population sampled. Helps interpret lab test results.
42
What is TSH?
Thyroid Stimulating Hormone produced by the pituitary ## Footnote Regulates thyroid hormone production; elevated in hypothyroidism, suppressed in hyperthyroidism.
43
What is LDL?
Low-Density Lipoprotein, known as 'bad cholesterol' ## Footnote Carries cholesterol to peripheral tissues and high levels are linked to atherosclerosis and cardiovascular disease.
44
What is albumin?
Main plasma protein produced by the liver ## Footnote Maintains oncotic pressure and transports various substances; low in liver disease, nephrotic syndrome, and malnutrition.
45
What is Urea?
A nitrogenous waste product formed in the liver; excreted by the kidneys. Elevated in renal dysfunction, dehydration, or high protein catabolism. ## Footnote Urea plays a crucial role in the body's nitrogen balance.
46
What are Electrolytes?
Crucial for fluid balance, nerve conduction, and acid–base status. Measured in a basic metabolic panel. ## Footnote Key electrolytes include Na⁺, K⁺, Cl⁻, and HCO₃⁻.
47
How is the Anion Gap calculated?
Na⁺ - (Cl⁻ + HCO₃⁻) ## Footnote Used to identify causes of metabolic acidosis like DKA and lactic acidosis.
48
What is the significance of Calcium (Total and Ionised)?
Essential for bone, nerve, and muscle function. Total Ca²⁺ is affected by albumin; Ionised Ca²⁺ is biologically active and abnormal in parathyroid disorders, CKD, malignancy. ## Footnote Ionised calcium is the form that participates in physiological functions.
49
What role does Phosphate (PO₄³⁻) play in the body?
Works with calcium in bone metabolism. Altered in CKD, vitamin D disorders, tumour lysis syndrome. ## Footnote Phosphate is critical for energy production and storage.
50
What is Cortisol?
Stress hormone produced by adrenal cortex. Measured in Cushing’s or Addison’s disease evaluation. ## Footnote Cortisol helps regulate metabolism and immune response.
51
What does HbA1c reflect?
Average blood glucose over ~3 months. Used for diabetes diagnosis and monitoring. ## Footnote HbA1c levels indicate long-term glucose control.
52
What is Insulin assessed for?
Hypoglycaemia workup and insulinoma. Can also be used to evaluate insulin resistance. ## Footnote Insulin is crucial for glucose metabolism.
53
What is the function of Parathyroid Hormone (PTH)?
Regulates calcium and phosphate. Measured in hyperparathyroidism or hypocalcaemia. ## Footnote PTH plays a key role in maintaining calcium homeostasis.
54
What does BNP / NT-proBNP indicate?
Released from ventricles in response to stretch. Marker of heart failure. ## Footnote Elevated levels suggest cardiac stress or failure.
55
What is Lipoprotein (a)?
An independent cardiovascular risk factor; elevated in premature atherosclerosis. ## Footnote Lipoprotein (a) is a genetic risk factor for heart disease.
56
What does Myoglobin indicate?
Early marker of muscle injury; released quickly post-MI but non-specific. ## Footnote Myoglobin can also indicate other muscle-related injuries.
57
What is High-sensitivity CRP (hs-CRP)?
Low-level inflammation marker used in cardiovascular risk prediction. ## Footnote Elevated hs-CRP levels may indicate systemic inflammation.
58
What does Alkaline Phosphatase (ALP) indicate when elevated?
Elevated in biliary obstruction, bone disease, or during pregnancy. ## Footnote ALP is important for diagnosing liver and bone disorders.
59
What is Alanine Transaminase (ALT)?
Liver-specific enzyme; elevated in hepatocellular damage. ## Footnote ALT is often used to assess liver health.
60
What does Aspartate Transaminase (AST) indicate?
Found in liver, muscle, and heart. Less specific than ALT. ## Footnote AST levels can indicate damage in multiple organ systems.
61
What does Gamma-Glutamyl Transferase (GGT) indicate?
Indicates cholestasis and alcohol-related liver injury. ## Footnote GGT is often elevated in liver disease.
62
What is Total Protein?
Sum of albumin and globulins; altered in malnutrition, liver disease, or plasma cell disorders. ## Footnote Total protein levels provide insight into overall health.
63
What is the Osmolar Gap?
Difference between measured and calculated osmolality. Used to detect toxic alcohol ingestion. ## Footnote A high osmolar gap may indicate the presence of unmeasured solutes.
64
What does eGFR stand for?
Estimated Glomerular Filtration Rate. Calculated from creatinine, age, sex, and ethnicity. ## Footnote eGFR is used to assess kidney function.
65
What are Free Light Chains (FLC)?
Sensitive markers for plasma cell dyscrasias (e.g., myeloma). ## Footnote FLC tests are important in the diagnosis and monitoring of multiple myeloma.
66
What do TIBC and Ferritin assess?
Used to assess iron stores. ## Footnote Ferritin indicates storage form (low in iron deficiency); TIBC is high in iron deficiency.
67
What is SIADH?
Excessive release of ADH despite normal/low plasma osmolality, leading to water retention and hyponatremia. ## Footnote SIADH stands for Syndrome of Inappropriate Antidiuretic Hormone Secretion.
68
What are the causes of SIADH?
* CNS disorders * Pulmonary diseases (e.g., pneumonia) * Malignancies (small cell lung carcinoma) * Drugs (SSRIs, carbamazepine) ## Footnote These causes can lead to the excessive secretion of ADH.
69
What is the pathophysiology of SIADH?
Increased water reabsorption in the collecting ducts → dilutional hyponatremia. ## Footnote This results in low plasma osmolality and inappropriately concentrated urine.
70
What are the lab findings in SIADH?
* Hyponatremia * Low serum osmolality * Inappropriately high urine osmolality (>100 mOsm/kg) * High urine sodium ## Footnote These findings are indicative of water retention and electrolyte imbalance.
71
What is the treatment for SIADH?
* Fluid restriction * Demeclocycline * Vasopressin receptor antagonists (vaptans) ## Footnote Treatment focuses on managing fluid balance and addressing the underlying cause.
72
What is Diabetes Insipidus (DI)?
Deficiency of ADH (central DI) or renal resistance to ADH (nephrogenic DI), causing polyuria and polydipsia. ## Footnote DI leads to excessive urination and thirst due to the inability to concentrate urine.
73
What are the causes of central Diabetes Insipidus?
* Head trauma * Pituitary surgery * Idiopathic ## Footnote These causes affect the production of ADH from the posterior pituitary gland.
74
What are the causes of nephrogenic Diabetes Insipidus?
* Lithium * Hypercalcemia * Chronic kidney disease ## Footnote These conditions affect the kidneys' response to ADH.
75
What is the pathophysiology of Diabetes Insipidus?
Impaired water reabsorption → excretion of large volumes of dilute urine → dehydration & hypernatremia. ## Footnote This leads to increased serum osmolality and risk of dehydration.
76
What are the lab findings in Diabetes Insipidus?
* High serum osmolality * Low urine osmolality (<300 mOsm/kg) ## Footnote These findings help differentiate between central and nephrogenic DI.
77
What test differentiates central vs nephrogenic Diabetes Insipidus?
Water deprivation test. ## Footnote This test assesses the kidneys' ability to concentrate urine in response to dehydration.
78
What is the treatment for central Diabetes Insipidus?
Desmopressin (ADH analog). ## Footnote Desmopressin mimics the action of ADH to reduce urine output.
79
What is the treatment for nephrogenic Diabetes Insipidus?
* Thiazide diuretics * Low-sodium diet * NSAIDs ## Footnote These treatments help improve kidney response to ADH.
80
What is Hungry Bone Syndrome?
Severe, prolonged hypocalcemia after parathyroidectomy (for hyperparathyroidism). ## Footnote This condition occurs due to sudden changes in calcium metabolism following surgery.
81
What is the pathophysiology of Hungry Bone Syndrome?
Sudden drop in PTH → increased calcium influx into bones → hypocalcemia, hypophosphatemia, hypomagnesemia. ## Footnote This results in the bones taking up calcium from the bloodstream.
82
What are the clinical features of Hungry Bone Syndrome?
* Tetany * Paresthesia * Muscle cramps ## Footnote These symptoms arise due to low calcium levels affecting neuromuscular function.
83
What are the lab findings in Hungry Bone Syndrome?
* Low calcium * Low phosphate * Low magnesium * Elevated ALP (bone turnover marker) ## Footnote These markers indicate bone metabolism and mineral imbalances.
84
What is the treatment for Hungry Bone Syndrome?
Calcium and vitamin D supplementation. ## Footnote This helps restore normal calcium levels and supports bone health.
85
What is Milk-Alkali Syndrome?
Hypercalcemia resulting from excessive intake of calcium and absorbable alkali (e.g., antacids) ## Footnote This syndrome is characterized by elevated calcium levels in the blood due to high consumption of calcium and substances that increase calcium absorption.
86
What are the main lab findings in Milk-Alkali Syndrome?
* Hypercalcemia * Metabolic alkalosis * Acute kidney injury (AKI) * Hypophosphatemia ## Footnote These lab findings are critical for diagnosing the syndrome and assessing its severity.
87
What is the treatment for Milk-Alkali Syndrome?
* Discontinue calcium/alkali * IV fluids * Bisphosphonates if severe ## Footnote Prompt treatment is essential to prevent complications associated with hypercalcemia and renal dysfunction.
88
What is Dilutional Hyponatremia?
Hyponatremia caused by excess free water relative to sodium, not true sodium depletion ## Footnote This condition occurs when there is more water in the body compared to sodium, leading to a dilution effect.
89
What are the causes of Dilutional Hyponatremia?
* SIADH * Heart failure * Liver cirrhosis * Nephrotic syndrome * Psychogenic polydipsia ## Footnote These conditions lead to water retention and ultimately dilute sodium levels in the bloodstream.
90
What are the lab findings associated with Dilutional Hyponatremia?
* Low serum sodium * Low serum osmolality * Variable urine sodium/osmolality depending on cause ## Footnote Understanding these lab findings helps differentiate dilutional hyponatremia from other types of hyponatremia.
91
What is the treatment approach for Dilutional Hyponatremia?
* Address underlying cause * Fluid restriction * Sometimes hypertonic saline ## Footnote Treatment should focus on correcting the underlying condition and managing fluid levels appropriately.
92
What is an Ion Selective Electrode (ISE)?
A method to measure electrolyte concentrations in serum/plasma (e.g., Na⁺, K⁺, Cl⁻) ## Footnote ISEs are crucial for accurate electrolyte assessment in clinical settings.
93
What is the principle behind Ion Selective Electrodes?
Electrochemical sensor selectively detects ion activity by potential difference across a membrane ## Footnote This principle allows for specific measurement of different ions in a solution.
94
What is the difference between Direct ISE and Indirect ISE?
* Direct ISE: Measures undiluted sample (used in blood gas analyzers) * Indirect ISE: Measures diluted sample (used in autoanalyzers, prone to pseudohyponatremia in hyperlipidemia/proteinemia) ## Footnote Understanding the differences is important for interpreting electrolyte results accurately.
95
What is the mechanism of action of Thiazide Diuretics?
Inhibit Na⁺/Cl⁻ symporter in the distal convoluted tubule → increased sodium and water excretion ## Footnote This mechanism is fundamental to the diuretic's effect on reducing blood volume and blood pressure.
96
What are the clinical uses of Thiazide Diuretics?
* Hypertension * Heart failure * Nephrolithiasis (calcium stones) ## Footnote Thiazide diuretics are commonly prescribed for these conditions due to their effectiveness in managing fluid balance.
97
What electrolyte effects are associated with Thiazide Diuretics?
* Hyponatremia * Hypokalemia * Hypomagnesemia * Hypercalcemia * Hyperuricemia * Hyperglycemia ## Footnote Monitoring these effects is essential for patient safety and managing potential complications.
98
What is the risk of Hyponatremia when using Thiazide Diuretics?
Increased water retention relative to sodium loss → dilutional hyponatremia ## Footnote This risk necessitates careful monitoring of sodium levels during treatment.
99
What should be regularly monitored in patients taking Thiazide Diuretics?
* Electrolytes (Na⁺, K⁺) * Renal function * Uric acid * Glucose ## Footnote Regular monitoring helps prevent and manage potential adverse effects of thiazide diuretics.
100
What is Diabetic Ketoacidosis (DKA)?
Acute, life-threatening complication of diabetes (mostly type 1) ## Footnote DKA is characterized by a triad of hyperglycemia, ketonemia, and acidosis.
101
What is the pathophysiology of DKA?
Absolute insulin deficiency → increased lipolysis → free fatty acids converted to ketone bodies → metabolic acidosis ## Footnote This sequence leads to the accumulation of ketones, resulting in acidosis.
102
What causes hyperglycemia in DKA?
Hyperglycemia → osmotic diuresis → dehydration, electrolyte imbalance ## Footnote This dehydration can lead to further complications if not treated promptly.
103
What are the clinical features of DKA?
Polyuria, polydipsia, nausea, vomiting, abdominal pain, Kussmaul respiration, fruity breath ## Footnote These symptoms are indicative of metabolic derangement and require urgent medical attention.
104
What are the laboratory findings in DKA?
Hyperglycemia (>13.9 mmol/L or 250 mg/dL), Ketonemia & ketonuria, High anion gap metabolic acidosis, Hyperkalemia ## Footnote Hyperkalemia occurs despite a total body potassium deficit.
105
What is the management for DKA?
IV fluids, insulin infusion, potassium replacement, correction of acidosis ## Footnote Each component is critical to stabilize the patient and correct metabolic derangements.
106
What is Hyperosmolar Hyperglycemic Nonketotic State (HONC / HHS)?
Severe hyperglycemia & dehydration without significant ketosis, seen in type 2 diabetes ## Footnote HHS is often triggered by infections or other stressors.
107
What is the pathophysiology of HHS?
Relative insulin deficiency prevents ketosis but inadequate to prevent hyperglycemia ## Footnote This leads to severe osmotic diuresis resulting in profound dehydration.
108
What are the laboratory findings in HHS?
Severe hyperglycemia (>33.3 mmol/L or 600 mg/dL), Serum osmolality >320 mOsm/kg, Minimal/absent ketones, Normal/slightly low pH & bicarbonate ## Footnote These findings highlight the significant dehydration and hyperosmolarity.
109
What is the management for HHS?
Aggressive IV fluids, insulin, electrolyte replacement ## Footnote Rapid rehydration is vital to prevent complications.
110
What is HbA1c?
Hemoglobin with glucose bound irreversibly to β-chain (non-enzymatic glycation) ## Footnote HbA1c is a key marker for long-term glucose control.
111
What is the clinical use of HbA1c?
Reflects average blood glucose over 2-3 months, Diagnosis of diabetes if ≥6.5% (48 mmol/mol) ## Footnote HbA1c testing is a standard method for monitoring diabetes management.
112
What are the advantages of using HbA1c?
Convenient (no fasting required) ## Footnote This makes it easier for patients to schedule testing.
113
What are the limitations of HbA1c?
Affected by hemoglobinopathies, anemia, rapid RBC turnover ## Footnote These factors can skew results and affect diabetes management decisions.
114
What is the Oral Glucose Tolerance Test (OGTT)?
Dynamic test to assess glucose handling ## Footnote It involves measuring fasting glucose, administering a 75g oral glucose load, and measuring glucose at 2 hours.
115
What is the procedure for the OGTT?
Measure fasting glucose, administer 75g oral glucose load, measure glucose at 2 hours ## Footnote This procedure helps in diagnosing diabetes and impaired glucose tolerance.
116
What glucose level indicates diabetes in the OGTT?
≥11.1 mmol/L at 2 hours ## Footnote This threshold is critical for diagnosing diabetes through the OGTT.
117
What glucose levels indicate impaired glucose tolerance?
7.8 - 11.0 mmol/L ## Footnote These values are used to assess the risk of developing diabetes.
118
What are the clinical uses of the OGTT?
Diagnosis of diabetes, gestational diabetes ## Footnote The test is particularly useful in screening for gestational diabetes.
119
What defines random glucose measurement?
Measured anytime ## Footnote This allows for the assessment of glucose levels regardless of the timing of the last meal.
120
What is the diabetes diagnosis threshold for random glucose?
≥11.1 mmol/L with symptoms ## Footnote Symptoms may include increased thirst, frequent urination, and fatigue.
121
What defines fasting glucose measurement?
After at least 8 hours fasting ## Footnote Fasting glucose is preferred for screening in asymptomatic patients.
122
What is the diabetes diagnosis threshold for fasting glucose?
≥7.0 mmol/L ## Footnote This level is critical for diagnosing diabetes in patients who are fasting.
123
What is hyperkalemia?
Serum potassium >5.0 mmol/L ## Footnote It indicates an imbalance in potassium levels that can have serious health implications.
124
What are common causes of hyperkalemia?
* Renal failure * Hypoaldosteronism * Acidosis * Cell lysis * Drugs (ACEi, ARBs, K⁺-sparing diuretics) ## Footnote These causes highlight the importance of monitoring potassium levels in at-risk patients.
125
What clinical features are associated with hyperkalemia?
* Muscle weakness * Arrhythmias * ECG changes (peaked T waves, widened QRS) ## Footnote These features are critical for identifying and managing hyperkalemia.
126
What is the first step in managing hyperkalemia?
Stabilize myocardium (calcium gluconate) ## Footnote This is crucial to prevent life-threatening cardiac events.
127
What methods can shift potassium intracellularly in hyperkalemia management?
* Insulin + glucose * Beta-agonists * Bicarbonate ## Footnote These treatments help to lower serum potassium levels quickly.
128
What are the methods to remove potassium in hyperkalemia?
* Diuretics * Dialysis ## Footnote These methods are used for more severe cases of hyperkalemia to prevent complications.
129
What is the definition of Metabolic Alkalosis?
Elevated blood pH due to increased bicarbonate (HCO₃⁻).
130
What are the causes of Metabolic Alkalosis?
* Vomiting * Nasogastric suction * Diuretics * Hyperaldosteronism
131
What is the compensatory response in Metabolic Alkalosis?
Hypoventilation to retain CO₂.
132
List clinical features of Metabolic Alkalosis.
* Muscle cramps * Weakness * Arrhythmias
133
What are the lab findings in Metabolic Alkalosis?
* Elevated HCO₃⁻ * Elevated pH * Compensatory rise in PaCO₂
134
What is the management for Metabolic Alkalosis?
Correct underlying cause, volume repletion with saline if chloride responsive.
135
What is the definition of Metabolic Acidosis?
Decreased blood pH due to decreased bicarbonate.
136
What are the two types of Metabolic Acidosis?
* High Anion Gap * Normal Anion Gap (Hyperchloremic)
137
What conditions are associated with High Anion Gap Metabolic Acidosis?
* DKA * Lactic acidosis * Renal failure * Toxins
138
What conditions are associated with Normal Anion Gap (Hyperchloremic) Metabolic Acidosis?
* Diarrhea * RTA
139
What is the compensatory response in Metabolic Acidosis?
Hyperventilation (Kussmaul respiration) to reduce CO₂.
140
What are the lab findings in Metabolic Acidosis?
* Low HCO₃⁻ * Low pH * Compensatory low PaCO₂
141
What is the management for Metabolic Acidosis?
Address underlying cause, bicarbonate therapy in severe cases.
142
What is Serum Creatinine?
Waste product of muscle metabolism, produced at a relatively constant rate. ## Footnote Used as a marker of renal function.
143
What does elevated Serum Creatinine indicate?
Kidney dysfunction, dehydration, muscle injury. ## Footnote Affected by muscle mass, age, sex, and hydration status.
144
What are the limitations of Serum Creatinine testing?
Can be normal in early kidney disease, not very sensitive for mild renal impairment. ## Footnote Its interpretation must consider individual factors.
145
What is Serum Urea (BUN)?
Waste product of protein catabolism, excreted by kidneys. ## Footnote Assesses renal function, hydration status, and protein metabolism.
146
What does elevated Serum Urea indicate?
Renal dysfunction, dehydration, high protein intake, GI bleeding. ## Footnote Decreased levels can indicate liver failure, malnutrition, or overhydration.
147
What are the limitations of Serum Urea testing?
Influenced by non-renal factors (diet, catabolism, hydration). ## Footnote Requires careful interpretation in context.
148
What is the Albumin-to-Creatinine Ratio (ACR)?
Ratio of urinary albumin to creatinine in a spot urine sample. ## Footnote Detects microalbuminuria, an early marker of kidney damage.
149
What are the interpretation ranges for ACR?
Normal: <3 mg/mmol, Microalbuminuria: 3–30 mg/mmol, Macroalbuminuria: >30 mg/mmol. ## Footnote Corrects for urine concentration variability.
150
What is the Estimated Glomerular Filtration Rate (eGFR)?
Estimated rate of blood filtration by glomeruli, calculated using serum creatinine, age, sex, and ethnicity. ## Footnote Gold standard for assessing kidney function and staging Chronic Kidney Disease (CKD).
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What are the normal and CKD staging ranges for eGFR?
Normal: >90 mL/min/1.73m²; CKD Stage 1 (>90), Stage 2 (60-89), Stage 3a (45-59), Stage 3b (30-44), Stage 4 (15-29), Stage 5 (<15). ## Footnote Limitations include inaccuracy in acute kidney injury and extremes of muscle mass.
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What is Alanine Aminotransferase (ALT)?
Liver enzyme involved in amino acid metabolism. ## Footnote Sensitive marker of hepatocellular injury.
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What does elevated ALT indicate?
Hepatitis, liver injury, fatty liver disease. ## Footnote More liver-specific than AST.
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What is a limitation of ALT testing?
May remain normal in chronic liver disease (e.g., cirrhosis). ## Footnote Requires comprehensive clinical correlation.
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What is Aspartate Aminotransferase (AST)?
Enzyme found in liver, heart, muscle, kidney. ## Footnote Marker of hepatocellular injury and sometimes muscle injury.
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What does elevated AST indicate?
Liver disease, myocardial infarction, muscle injury. ## Footnote Less specific to liver compared to ALT.
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What does an AST:ALT ratio of 2:1 suggest?
Alcoholic liver disease. ## Footnote A ratio of <1 is indicative of viral hepatitis.