Endocrinology Flashcards
Etiology of hypoglycaemia can be defined into two broad categories?
- Insulin-mediated
2. Insulin Independent
Ddx for insulin-mediated hypoglycaemia?
- Exogenous administration of insulin
- Insulin secretagogue use
- Insulin-secreting tumors (insulinomas, nesidioblastosis)
- Post-bariatric surgery hypoglycemia
- Insulin autoimmune hypoglycemia
What is an insulinomas
Insulinoma is a rare neuroendocrine tumor of insulin producing beta cells
What is an nesidioblastosis?
Nesidioblastosis is hypertrophy of insulin-producing beta cells in the pancreas.
Ddx for insulin independent hypoglycaemia?
- Malnutrition or starvation
- Cirrhosis/Hepatic Failure
- Sepsis
- End-stage renal disease
- Advanced heart failure
- Adrenal insufficiency
- Hormone deficiency (cortisol, glucagon and epinephrine in insulin-deficient DM)
- Non-islet cell tumours (typically the result of mesenchymal tumour overproduction of IGF-II)
- Inborn error of carbohydrate metabolism, glycogen storage disease, gluconeogenic enzyme
- Alcohol
- Drugs (e.g. quinine, indomethacin, gatifloxacin, lithium, ACE inhibitors, β-adrenergic receptor blockers)
How does pseudohypoglycemia occur?
Pseudohypoglycemia occurs when processing of blood specimens in untreated test tubes is delayed and cells, such as red blood cells and leukocytes (especially if increased, as in leukemia or polycythemia), consume glucose. Poor circulation to the digits can also cause erroneously low fingerstick glucose measurements.
What are the symptoms of hypoglycaemia?
- Autonomic nervous system activity – palpitations, sweating, tachypnea, tachycardia
- Neuroglycopenic symptoms – caused by decreased activity of CNS – dizziness, headache, clouding vision, mental dullness, fatigue, confusion, seizures
The surge in _______ in response to low plasma glucose typically occur first in hypoglycaemia
Autonomic activity
What is Whipple’s triad which suggest a patient’s symptoms are from hypoglycemia?
- serum glucose <4.0 mmol/L
- neuroglycopenic symptoms (confusion, sensation of warmth, weakness or fatigue, severe cognitive failure, seizure, coma)
- rapid relief provided by administration of glucose
Investigations of hypoglycaemia?
When the cause of hypoglycemia is not evident, screen for oral hypoglycemic agents and measure plasma glucose, serum ketones, insulin, pro-insulin, C-peptide, and insulin antibodies during a spontaneous hypoglycemic episode or a supervised fast of up to 72 h
What is C-Peptide?
A short peptide released into the circulation when proinsulin is cleaved to insulin
How can C-Peptide be used to distinguish between Exogenous and Endogenous source of hyperinsulinemia
o Increased = endogenous
o Decreased or normal = exogenous
Treatment for mild to moderate hypoglycemia (autonomic and neuroglycopenic symptoms)?
Rule of 15s:
- Ingestion 15g carbs (glucose tabs)
- Wait 15 mins - Check BG again
- If <4 repeat dose of carbs
Treatment for severe (unconscious) hypoglycemia?
Glucagon 1mg (IM or SC) or 1 amp D50W IV
After initial management of hypoglycaemia what are the next steps?
- Get them a complex snack afterward
2. Reduce their insulin dose
What is hypoglycemic unawareness?
Patient remains asymptomatic until severely hypoglycemic levels are reached
Etiology of hyperglycemia?
- Diabetes – impaired glucose tolerance, T1Dm, T2DM, gestational diabetes
- Endocrinopathy - Cause peripheral insulin resistance like Cushing syndrome, acromegaly, and pheochromocytoma
- Meds - corticosteroids, estrogen, beta blockers, epinephrine, thiazide diuretics, niacin, pentamidine
- Destruction of the pancreas from chronic pancreatitis, hemochromatosis, pancreatic cancer, and cystic fibrosis
- Total parental nutrition and dextrose infusion
- Critical Illness/Physiologic Stress – acute pancreatitis, post-stroke, post MI, shock, stress hyperglycemia (trauma, surgery, burns)
What are the causes of hypoglycemic unawareness?
- Decreased glucagon/epinephrine response
- History of repeated hypoglycemia or low HbA1c
- Autonomic neuropathy
What are the risk factors of hypoglycemic unawareness?
RFs: elderly, renal impairment, thin, missed meals, exercise, insulin, secretagogues
What is the treatment of hypoglycemic unawareness?
Tx: Get them to higher BG levels (>12) so their thermostat can reset and therefore notice their lows
Physical exam for hyperglycemia?
- General – ABCs
- Airway: GCS
- Breathing – monitor for Kussmaul breathing (rapid and deep respiration), fruity acetone breath (DKA)
- Circulation – postural BP and HR, assess JVP, mucous membranes, urine output and capillary BG - DERM – hyperpigmentation of the skin (r/o Addison’s disease)
- ABDO: abdominal tenderness (DKA)
- NEURO
Investigations for hyperglycemia?
Investigations: urinalysis/urine ketones, TSH, troponin, ABG, plasma glucose, lytes, Cr, bicarb, beta-hydroxybutyrate, CBC, urine/blood culture, amylase/lipase, plasma osmolality
- CXR
Describe the pathophysiology of diabetic ketoacidosis.
Insulin deficiency causes the body to metabolize triglycerides and amino acids instead of glucose for energy. Serum levels of glycerol and free fatty acids rise because of unrestrained lipolysis, as does alanine because of muscle catabolism. Glycerol and alanine provide substrate for hepatic gluconeogenesis, which is stimulated by the excess of glucagon that accompanies insulin deficiency.
Glucagon also stimulates mitochondrial conversion of free fatty acids into ketones. Insulin normally blocks ketogenesis by inhibiting the transport of free fatty acid derivatives into the mitochondrial matrix, but ketogenesis proceeds in the absence of insulin. The major ketoacids produced, acetoacetic acid and beta-hydroxybutyric acid, are strong organic acids that create metabolic acidosis.
The increase H is exchanged for potassium and thus causes hyperkalemia and eventually excreted. The potassium stores inside the body will therefore run low.
Causes of diabetic ketoacidosis?
Causes: insulin omission, infarction (MI, CVA), iatrogenic (steroids), new Dx, infection (stress increases release of epinephrine which releases glucagon which will result in increased blood glucose, loss of glucose in the urine and loss of water and therefore dehydration. You will also need alternative energy – generation of ketone bodies – ketoacidosis.
Symptoms of diabetic ketoacidosis?
Sx: weight loss, nausea, vomiting, abdominal pain, dehydration, hypotension, tachycardia, LOC, polyuria, blurry vision, nocturia
• Kussmaul resp (deep/labored breathing in an attempt to reduce CO2 – reduce acidity).
Diagnostic criteria for diabetic ketoacidosis?
Plasma glucose hyperglycemia 14-35 mmol/L, ketones in either blood or urine, metabolic acidosis pH <7.3 ABG, serum bicarb <15 mmol/L, anion gap > 14 mmol/L
Describe the treatment orders for diabetic ketoacidosis?
Diet: NPO
Activity: Limit to bed rest until resolution
Vitals and Neuro vitals: Q1H for first 4 hours, then Q2-4H until resolution
IV fluids:
Determine hydration status:
- Hypovolemic Shock: NS at 1-2L/hr until stable
- Mild/moderate dehydration: NS 500cc x4hr then 250cc x2hr
- When BG 12-14 mM, switch to 0.45% NaCl + 5% dextrose @ 250 cc/hr
Insulin:
Potassium:
Bicarbonate:
Accurate ins/outs +/- foley catheter
If pH <7.0 in DKA, 44.6 mM of _____ in 200cc of sterile water and infuse at 200cc/hr Q2H until pH >7.0
Sodium bicarbonate
Describe the management of insulin in DKA
o Hyperglycemia is corrected by giving regular insulin 0.1 unit/kg IV bolus initially, followed by continuous IV infusion of 0.1 unit/kg/hour in 0.9% saline solution.
o Check BG hourly, if BG does not fall >3 mM in first hr, check hydration level and double insulin every hour until BG drops 3-4 mM per hour.
o When plasma glucose becomes < 11.1 mmol/L in adults, 5% dextrose should be added to IV fluids to reduce the risk of hypoglycemia. Insulin dosage can then be reduced to 0.02 to 0.05 unit/kg/hour and should be maintained until the anion gap has narrowed and blood and urine are consistently negative for ketones.
o Insulin replacement may then be switched to regular insulin 5 to 10 units subcutaneously every 4 to 6 hours.
o When the patient is stable and able to eat, a typical split-mixed or basal-bolus insulin regimen is begun. IV insulin should be continued for 1 to 4 hours after the initial dose of subcutaneous insulin is given.
When can you determine that DKA is resolved?
BG <14mM, bicarbonate >15 mM, venous pH >7.3 and anion gap <12mM
Complications of DKA?
Complications: cerebral edema, acute respiratory distress, sepsis, MI, hypokalemia (Insulin causes K to shift from blood into cells, which can cause hypokalemia which can cause an arrhythmia)→ arrhythmia, hypoglycemia, mortality 1-2%
Describe the management of potassium in DKA
o Hyperkalemia b/c acidosis drives potassium out of cells initially, but the glucose causes diuresis which causes potassium to be excreted in urine and insulin treatment causes K into cells
o Hypokalemia prevention requires replacement of 20 to 30 mEq (20 to 30 mmol) potassium in each liter of IV fluid to keep serum potassium between 4 and 5 mEq/L (4 and 5 mmol/L).
o If serum potassium is < 3.3 mEq/L (3.3 mmol/L), insulin should be withheld and potassium given at 40 mEq/hour until serum potassium is ≥ 3.3 mEq/L (≥ 3.3 mmol/L);
o If serum potassium is > 5 mEq/L (> 5 mmol/L), potassium supplementation can be withheld.
Definition of hyperosmolar hyperglycemic syndrome (HHS/HONK)?
Hyperglycemia, increased plasma osmolality, negative ketones
Describe the pathophysiology of hyperosmolar hyperglycemic syndrome (HHS/HONK).
- It usually develops after a period of symptomatic hyperglycemia in which fluid intake is inadequate to prevent extreme dehydration due to the hyperglycemia-induced osmotic diuresis.
- Serum ketones are not present because the amounts of insulin present in most patients with type 2 diabetes are adequate to suppress ketogenesis. Because symptoms of acidosis are not present, most patients endure a significantly longer period of osmotic dehydration before presentation, and thus plasma glucose (> 600 mg/dL [> 33.3 mmol/L]) and osmolality (> 320 mOsm/L) are typically much higher than in diabetic ketoacidosis.
Precipitating factors of hyperosmolar hyperglycemic syndrome (HHS/HONK).
- Acute infections and other medical conditions
- Drugs that impair glucose tolerance (glucocorticoids) or increase fluid loss (diuretics)
- Nonadherence to diabetes treatment
Symptoms of hyperosmolar hyperglycemic syndrome (HHS/HONK)?
The primary symptom of hyperosmolar hyperglycemic state is altered consciousness varying from confusion or disorientation to coma, usually as a result of extreme dehydration with or without prerenal azotemia, hyperglycemia, and hyperosmolality.
Treatment for hyperosmolar hyperglycemic syndrome (HHS/HONK)?
• ABCs
• IV 0.9% saline - At a rate of 15 to 20 mL/kg/hour, for the first few hours. After that, the corrected sodium should be calculated. If the corrected sodium is < 135 mEq/L (< 135 mmol/L), then isotonic saline should be continued at a rate of 250 to 500 mL/hour. If the corrected sodium is normal or elevated, then 0.45% saline (half normal) should be used.
• Correction of any hypokalemia - similar to that in diabetic ketoacidosis: 40 mEq/hour for serum potassium < 3.3 mEq/L (< 3.3 mmol/L); 20 to 30 mEq/hour for serum potassium between 3.3 and 4.9 mEq/L (3.3 and 4.9 mmol/L); and none for serum potassium ≥ 5 mEq/L (≥ 5 mmol/L).
• IV insulin (as long as serum potassium is >3.3 mEq/L [>3.3 mmol/L])
o Safe to stop insulin drip after: long acting SC injection (0.2U/kg), 2 successful normal anion-gaps, and pt able to eat food by mouth
Definition of DM?
Diabetes mellitus is a heterogeneous metabolic disorder characterized by the presence of hyperglycemia due to impairment of insulin secretion, defective insulin action, or both
List the 4 ways to diagnosis DM?
o Fasting plasma glucose > 7.0 mmol/L OR
o HbA1C > 6.5% in adults OR
o 2h plasma glucose in 75g OGTT > 11.1 mmol/L OR
o Random plasma glucose > 11.1 mmol/L
o In the presence of hyperglycemia symptoms (polyuria, polydipsia, polyphagia, weight loss, blurry vision), a confirmatory test is not required
o In the absence of hyperglycemic symptoms, a repeat confirmatory test (FPG, A1C, 2h PG in a 75g OGTT) done on another day is required for diagnosis of diabetes
HbA1c for pre-diabetes?
A1c > 6.0%
What does HbA1c reflect?
Reflects glycemic control over 3 mo and is a measure of patient’s long-term glycemic control
What are the symptoms of diabetes?
Incidental finding of hyperglycemia (polydipsia, polyuria, nocturia, blurred vision, fatigue, poor concentration, recurrent infections (yeast), weight loss→ suggests insulin deficiency), osmotic Sx, medical emergency (DKA, Coma)
What should be done on physical exam for DM?
o Vitals: BP/orthostatic hypotension (diabetic autonomic neuropathy), HR/delayed postural HR response, RR. BP goal <130/80 mmHg
o Hands: Stiff hands + prayer signs (limited joint mobility or diabetic cheiroarthropathy), Dupuytren’s contracture. Assess for burning, paresthesias, sensory loss in the median nerve distribution, positive Tinel’s and Phalen’s test (carpal tunnel syndrome)
o Derm: Inspect for presence of infections
o HEENT: Acanthosis nigricans, JVP
o Eyes: Pupillary response to light, EOM, fundoscopy. Should see ophthalmology
o CV: palpation – assess for carotid and femoral artery bruits, peripheral artery pulses. Auscultate – ventricular dysfunction (diabetic cardiomyopathy)
o Feet: Assess for diabetic foot
What are the investigations for DM?
Lytes, CBC, UA, serum ketones, HCG (if F)
When is the typical onset of T1DM
Onset: Usually <30 yr of age
What percentage of cases of T1DM have no family Hx?
90% of cases no family Hx
T1DM is associated with which MHC class II cell surface receptor?
Associated with HLA-DR-DQ
Define T1DM
Beta cell destruction by lymphocytic infiltrates, typ. leading to absolute insulin deficiency, can be autoimmune or idiopathic
Target for T1DM
Target might be between 7.1-8.5% with limited life expectancy
Mainstay treatment for T1DM?
Insulin replacement
How do you calculate the total daily dose of insulin?
To calculate total daily dose is 0.3 unit per kg of body weight. (40-50% basal, 50-60% bolus – basal-bolus insulin therapy, more physiologic, bolus insulin often given with meals, promotes glucose utilization + uptake after meal, controls postprandial glucose)
What is Type 2 diabetes mellitus?
Peripheral insulin resistance +/or insulin deficiency
Typical onset for T2DM?
Usually >40 yr of age. Increasing incidence in pediatric population 2o to obesity
Risk factors for T2DM?
Risk factors: central obesity, sedentary lifestyle, family Hx, ethnicity (aboriginal, Hispanics, black), gestational diabetes, acanthosis nigricans
Initial management of T2DM with A1c <8.5%?
If initial A1c <8.5% → metformin or reassess 2-3mos. Initiate non-insulin antihyperglycemic therapy within 2-3m if lifestyle (diet, exercise, smoking cessation) does not result in glycemic control.
1st choice treatment option of T2DM
Metformin
Initial management of T2DM with HbA1c >8.5%?
If initial HbA1c >8.5% at time of diagnosis, initiate pharmacologic therapy with metformin immediately and consider combination of therapies
S/E of metformin?
Biggest S/E is diarrhea, anorexia, lactic acidosis
Absolute contraindications of metformin?
ABSOLUTE: Moderate to severe liver dysfunction. Moderate renal dysfunction GFR <30 mL/min. Cardiac dysfunction
What are the insulin secretagogues
Sulfonylureas, meglitinides
S/E of the insulin secretagogues?
S/E: Hypoglycemia. Weight gain.
Absolute contraindications of the insulin secretagogues?
Moderate to severe liver dysfunction
Interactions of the insulin secretagogues?
Do not combine with a non-sulfonylurea insulin secretagogue or preprandial insulin.
Benefit/advantage of metformin?
No hypoglycemia or weight loss, can combine with insulin
What are thiazolidinediones (TZDs)?
Insulin sensitizers
Benefit/advantage of thiazolidinediones (TZDs)?
No hypoglycemia risk
Absolute contraindications of thiazolidinediones (TZDs)?
NYHA > class II CHF
Interactions of thiazolidinediones (TZDs)?
Do not combine with insulin
Risk of SGLT-2 inhibitors?
Cause euglycemic DKA
Absolute contraindications of SGLT-2 inhibitors?
Severe renal impairment, ESRD, patients on dialysis
How do alpha glucose inhibitors work?
Acarbose: slows digestion of oligosaccharides→ monosaccharides, slows delivery of glucose to circulation
Biggest down side to alpha glucose inhibitors?
Poorly tolerated – diarrhea and gas
Target of BP with DM?
Target: <130/80
First-line therapy for type 1 and type 2 diabetic patients with microalbuminuria, even if they are normotensive?
ACEi or ARB
Target for LDL in patients with DM?
Target: LDL <2.0mmol/L
Which diabetic patients should be on a statin?
Statin therapy if >40yo OR macro/microvascular disease OR long duration of DM (>15 yrs and >30 y/o)
How to screen for CKD in diabetic patients
Screen with serum creatinine and random urine ACR + urinalysis
- T1DM – exam 5 years post Dx and then annually
- T2DM – exam at Dx and then annually
Target of ACR for diabetic patients
Target: Normal ACR <2.0 mg/mmol/L
How to screen for retinopathy in diabetic patients
- Investigations: Direct ophthalmoscope - neovascularization or vitreous hemorrhage; macular edema
- Follow-Up:
• T1DM – exam 5 years post Dx and then annually
• T2DM – exam at Dx and then 1-2 years if no retinopathy
What is autonomic neuropathy?
Resting tachycardia, postural hypotension, ED, abnormal sweating, gastroparesis, constipation/diarrhea
What is distal symmetrical sensory peripheral neuropathy?
Glove + stocking distribution, foot ulcers, amputations
S/S of neuropathic foot ulcers?
Plantar, pressure areas associated callus, painless, warm feet with dilated veins
S/S of ischemic foot ulcers?
Dorsum/lateral, painful, punched out, cold, pale, pulseless
What is Charcot foot?
Destruction of bony structure, consequence of neuropathy
Target for glycemic control in the hospital?
6-10 mmol/L is target for glycemic control
What test can you do to determine whether patient has T1DM or T2DM?
A normal C-peptide range is 0.5 to 2.0 nanograms per milliliter.
These levels can be high when your body makes more insulin than usual. Levels are low when your body makes less than it normally should.
Insulin complications
Weight gain, hypoglycemia, lipohypertrophy, lipoatrophy, insulin allergy
How to calculate insulin requirements in hospital?
• TIDM = Weight (kg) x 0.15-0.3 – Total Daily Dose
• T2DM = Weight (kg) x 0.3-0.5 – Total Daily Dose
• Then divide the TDD in half = basal 50%, bolus 50%.
o Bolus divide by 3 for peri prandial
Definition of short stature
Definition: height is 2 standard deviations (SD) or more below the mean for children of that sex and chronologic age
Etiology of short stature?
ABCDEFG Alone (neglected infant) Bone dysplasias (rickets, scoliosis, mucopolysaccharidoses) Chromosomal (Turner, Down) Delayed growth (constitutional) Endocrine (low GH, Cushing, hypothyroid) Familial GI malabsorption (celiac, Crohn’s) IUGR
What distinguishes Familial Short Stature with Constitutional Delay of Growth?
Normal bone age - consistent with chronological age
Are pre-pubertal and pubertal growth velocities normal or abnormal in Familial Short Stature?
Normal pre-pubertal and pubertal growth velocity, short parents, normal timing of pubertal onset - final height within expected range without intervention
Are pre-pubertal and pubertal growth velocities normal or abnormal in Constitutional Delay of Growth/Puberty?
Normal pre-pubertal growth velocity but late onset of puberty.
What is the hallmark of Constitutional Delay of Growth/Puberty?
Delayed skeletal age; growth typically continues LONGER than normal, but results in adult stature within normal range
Should children with Constitutional Delay of Growth/Puberty achieve normal final height without intervention?
Yes
What is idiopathic short stature?
Height < 2 standard deviations below the mean for age with no identified pathology, normal growth velocity and bone age
What are the normal variants of growth for short stature?
- Familial Short Stature
- Constitutional Delay of Growth/Puberty
- Idiopathic short stature
What are the pathologic causes for short stature?
- Undernutrition
- Glucocorticoid therapy
- Chronic diseases: Celiac disease, GI disease, Rheumatologic disease (JIA), Chronic kidney disease
- Endocrine: Achondroplasia, Cushing syndrome, Acquired GH deficiency, Congenital growth hormone deficiency, Hypothyroidism
- Genetic disease: Turner syndrome, SHOX gene variants, Prader-Willi syndrome
What is the hallmark of undernutrition?
The hallmark of undernutrition is low weight-for-height.
What are the symptoms seen with Celiac disease?
Abdominal pain, malabsorption, anemia; short stature may be the only symptom
Children with growth failure resulting from gastrointestinal disease tend to have a greater deficit in _____ in contrast to those with endocrine disorders, who are often ______.
Children with growth failure resulting from gastrointestinal disease tend to have a greater deficit in weight than height (ie, they are underweight-for-height) in contrast to those with endocrine disorders, who are often overweight-for-height
Symptoms + signs of achondroplasia?
Short limbs; long, narrow trunk; large head with prominent forehead
Most common cause of Cushing syndrome?
The most common cause is a corticotropin (ACTH)-secreting pituitary adenoma (Cushing disease)
Best test to establish diagnosis of Cushing syndrome?
The best tests to establish the diagnosis are a 24-hour urine collection for free cortisol (and creatinine), or a dexamethasone suppression test
What risk factors would make you think acquired GH deficiency?
History of head trauma or cranial irradiation, central nervous system infection
Features of Turner syndrome?
Turner syndrome: Short stature, webbed neck, characteristic facies, short metacarpals, broad chest with widely spaced nipples, hyperconvex fingernails and toenails; may be normal appearing; decreased growth velocity and delayed puberty
Features of congenital growth hormone deficiency?
Hypoglycemia, birth length may be normal, height and bone age progressively delayed; jaundice, microphallus, midline craniofacial abnormalities
What should be obtained on history for short stature?
Determine: onset of short stature, i.e. the need to change shoe/clothing sizes, relative height difference between peers and siblings + dietary history
BIND History: prenatal history, delivery weight/length/GA, any IUGR/SGA/prematurity, neonatal hypoglycemia or prolonged jaundice, developmental history
PMHx + Pubertal Onset Hx + Medications: corticosteroid or stimulant use
FMHx: family members’ heights + pubertal history calculate target height (mid parental height)
ROS: for systemic diseases – GI, cardiac, renal, hypothyroid, neuro
Risk factors for GH deficiency?
Previous head trauma, history of intracranial bleed or infection, head surgery or irradiation, positive family history, breech delivery
What should be done on physical exam for short stature?
- Calculate mid-parental height: children are usually in a percentile between their parents’ height
- Tanner Staging: assess pubertal development
How do you calculate mid-parental height?
(mid-parental height = (mother + father’s height in cm ± 13cm)/2) - normal children should be within 10cm of this target
How do you confirm bone age for constitutional delay?
Confirm with bone age XR - AP x-ray of left hand and wrist for bone age
Investigations for short stature
CBC (anemia), CRP (IBD), Follicle-stimulating hormone, karyotyping (Turner), Insulinlike growth factor 1 (GH deficiency), TSH, free T4 (hypothyroidism, UA (renal disease), Tissue transglutaminase and total immunoglobulin A (celiac)
______ is approved for a variety of conditions that cause short stature, including Turner syndrome, chronic renal failure, Prader-Willi syndrome, small for gestational age, Noonan syndrome, short stature homeobox-containing gene deficiency, and idiopathic short stature.
Recombinant growth hormone
Definition for intrauterine growth restriction?
Definition: <10th%ile fetus that has not reached its growth potential. Infant weight <10%ile for GA or <2500g or abdominal circumference <10%ile.
What are the 3 types of IUGR?
- Symmetric IUGR – Type 1 1A: constitutional (small women) 1B: intrinsic - Asymmetric IUGR – Type 2 - Indeterminate IUGR – Type 3
What are the causes of symmetric IUGR - Type 1?
Congenital or TORCH
Is symmetric IUGR - Type 1 early or late gestational onset?
Growth inhibition early in gestation due to fetal abnormalities/insult. Inhibition of active mitosis, affecting cell hyperplasia.
What are the causes of asymmetric IUGR - Type 2?
Placental insufficiency (redistribution of blood to critical organs: brain, heart, adrenals preserved, brain sparing effect) or external factor – brain/heart/adrenals spared, ^MCA doppler =
What are the causes of indeterminate IUGR – Type 3?
Maternal vascular disease (lupus, HTN)
Does indeterminate IUGR – Type 3 affect cell hypertrophy or cell hyperplasia?
Decrease in cell hypertrophy and cell hyperplasia.
