Primary Care - Metabolic Disorders - DM, Hyperkalemia, Hypokalemia, Hypernatremia and Hyponatremia, Lipid Disorders, Metabolic Syndrome and Thyroid
Terms in this set (102)
DM Type II
Manifests as nonketotic hyperglycemia due to insulin resistance
Impaired insulin secretion
DM Type II -- Initial RFs and manifestations
Typically patient over 40 years of age
Presents with polyuria and polydipsia
Yeast infection may be first manifestation (due to urine ketones)
Often few or no symptoms
What is the Fasting Glucose of DM II?
Fasting at or above 126 more than once OR
Glucose at or above 200 tw0-hours after 75 gram of oral glucose
DM II is associated with what disorders?
Patho of DM II
Peripheral insulin resistance
Defective insulin secretion, esp in response to a glucose stimulus
Strong genetic influences
What enhances DM II? (Risk Factors)
HX of GD with a birthweight > 9#
High Tri's and low HDL
Ethnicity -- AA, latino, native american, Asian, Pacific islander
Abdominal fat with an abnormally high waist-hip ratio is generally associated with obesity in type 2 diabetes.
Drug-chemical induced -- chemo, glucoticoids, atypical antipsychotics
Correlates with insulin resistance, whereas subcutaneous fat seems to have less of an association.
DM II - HISTORY
DM II - Physical Exam
Abdominal Exam for hepatomegaly
Focused Neuro Exam
Diabetic foot exam
DM II - Testing/Labs
HA1C - > 6.5% is diagnostic
Hyperglycemia crisis + random plasma glucose >200 mg/dL or fasting PG >126 mg/dL on 2 occasions OR
2 hour plasma glucose >200 mg/dL during an oral glucose tolerance test (OGTT) with 75g glucose load.
Diagnosis of DM II
Based on labs
Lipoprotein abnormalities - trigs 300-400, HDL 30 or less and high LDL (Different than type I, slight elevation in LDL and trigs and minimal change in HDL)
DM II - Treatment
First line --> Biguanides
1. Metformin 500-2000 mg in divided doses or ER 1000-2000 mg every HS - Max is 2000 mg/d
2. Sulfonylureas --> Glipizide (Glucotrol) 2.5-40mg/d - given before meals (multiple different formulations, ER etc)
3. Thiazolidinediones --> (Actos): 15-45 mg/d
4. A-Glucosidase inhibitors --> (Precose) Acarbose 25-100 mg TID - Poor patient adherence due to GI symptoms - also must be taken at the beginning of a meal to prevent postprandial hyperglycemia.
Which medication may stimulate the risk of bladder cancer?
Which medication may increase the risk of MI, CVA or PE?
Avandia - Rosiglitazone (Thiazolidinediones)
Which labs need to me monitored when prescribing a thiazolidinediones?
Serum Transaminases every 2 months for the first year and is contraindicated in patients with liver disease and symptomatic heart failure.
What is the target A1C for DM II?
Less than 7.0 or 6.5 without significant hypoglycemia
Less than 8.0 with limited life expectancy or with micro-macrovascular complications.
Why is Metformin first line of therapy for DM II?
Because of weight loss and insulin resistance.
Use in caution with patients with renal insufficiency, prior to contrast use, surgery and severe acute illness.
Caution in CHF patients
Which drugs stimulate insulin secretion?
Which drugs alter insulin action?
Which drugs affect glucose absorption?
Which class of drug is avoided in a patient with renal insufficiency, IBD, colonic ulceration and partial bowel obstruction?
What are the treatment goals for DM Type II?
Pre-prandial BS - 80-120
HS Blood Sugar - 100-140
Post-prandial - < 180
HAIC - <7.0%
What are the other considerations regarding DM type II?
Screen for microalbuminuria annually (UA)
Annual Foot exam
Diabetic eye exam at least annually
Monitor infections of skin and mucus membranes
Eruptive xanthomas from HIGH trig is associated with poor diabetic control
Need good hypertensive control
What is the hallmark of DM II?
Insulin resistance - however beta cell dysfunction is also present.
When would an A1C be inaccurate?
When the patient is anemic, pregnant, or suffers from some hemoglobinopathy
What is the LDL goal with patients with preexisting CVD or risk factors for CVD?
LDL of <70
Low dose aspirin should be prescribed for all adults?
T or F
What is the first line of drug for hypertension and kidney protection?
ACEI or ARB --- if contraindicated may consider a calcium channel blocker.
What is the BP goal of a DM type II patient?
Hypercalcemia refers to what?
Serum CA greater than 10.2mg/dL
Mild <12mg/dL are typically without symptoms
Severe 14mg/dL and above -- considered crisis
Where is hypercalcemia typically seen?
Critically ill patients
Symptoms R/T hypercalcemia?
2. Neurological --
3. Renal --
Complaints related to oliguric renal failure
Chronic, complaints related to:
4. GI --
Chronic, complaints related to:
Peptic ulcer disease
5. Dermatologic --
Mnemonic: "Stones, Bones, Groans, Thrones and Psychiatric Overtones," "bones" refers to bone pain and "thrones" refers to polyuria.
Physical Exam of HyperCAL?
- Patient may appear irritable, lethargic, stupor, coma or hyporeflexia.
- Hypotensive if dehydrated
- Sinus Brady
- Derm exam may show band keratopathy or ectopic calcification
Labs for HyperCAL?
Vit D metabolites
Dig level if indicated
Thyroid function tests
HyperCAL treatment includes --
Fluids to reduce CA level - isotonic saline 200-300 ml/hr
Hypocalcemia refers to?
Defined as a total plasma calcium level <8.7 mg/dL
Ionized calcium may be normal and, therefore, have no clinical manifestations.
Normal total serum calcium concentrations are 8.7-10.5 mg/dL.
Etiology of HypoCal?
Hypoalbuminemia—the most common cause
Presentation of HypoCal?
Neuromuscular - Paresthesias
Muscle spasms, weakness and cramping
Choreoathetosis (involuntary movements)
Cardio - Torsades de pointes
What ECG changes are seen on HypoCAL
QT and ST prolongation
What psychiatric symptoms are associated with HYPOCAL?
What ocular symptoms are R/T to HYPOCAL
Initial Labs/Testing for HYPOCAL?
BUN/CR and glucose
Serum calcitriol levels
What does an increase in phosphate levels indicated?
What does a decrease in phosphate levels indicate?
Vit. D defiency
When is treatment immediate?
If serum calcium is below 8.0mg/dl and is symptomatic (muscle cramping or stridor)
METABOLIC syndrome - Defined
A cluster of metabolic abnormalities that confer an increased risk factor for type 2 diabetes, CVD, stroke, fatty liver and certain cancers.
METABOLIC syndrome involves what other association conditions?
Insuline resistance with or without impaired glucose tolerance
Pro inflammatory state
RFs of METABOLIC syndrome?
Alterations of gut flora
Etiology METABOLIC syndrome
Obesity - particularly abdominal
Other contributing factors--
Endocrine (post menopause)
HX of METABOLIC
Family HX of DM Type II
Symptoms R/T to CVD or diabetes
Comprehensive lifestyle HX including --> diet, carb versus fat intake. Weight hx, onset of obesity and previous weight loss attempts. Exercise regimen and alcohol intake.
PE of METABOLIC
According to the ATP III a diagnosis can be made with 3 or more characteristeric --
HDL - men <40 and women <50
Fasting glucose >100 mg/dl
Labs for METABOLIC
Fasting lipids - including TGs and HDL
Other labs may reveal what for METABOLIC?
Increased WBC count
Increased C-reactive protein
Increased pro inflammatory cytokines
Increased uric acid
Type 2 DM
HTN and/or diabetic eye disease
Peripheral vascular disease
TX of METABOLIC
Prevent and reduce obesity. Aggressive lifestyle modifications diet and exercise is FIRST line!
Medications for METABOLIC
TX for related diseases
What labs needed to be checked before prescribing a statin?
Baseline liver enzymes pre-treatment and 6-8 weeks after the start of treatment.
When should therapy for statins be modified or stopped?
If 2-2.5 times normal elevation of the liver enzymes - consider issues such as alcohol intake
When is consultation or referral necessary?
When the patient is resistant to therapy despite trial with different medicines.
F/U recommendations for METABOLIC?
Regular 30 minute exercise will improve all components of METABOLIC (Small periods of time several times a day is just a beneficial).
Regular monitoring of weight, abdominal circumference measurements, BP, fasting lipids, and sugar levels.
HYPERKALEMIA - defined
Plasma potassium greater than 5.5 mEq/L.
High K+ depresses cardiac conduction
Leads to fatal arrhythmias
What are the four major causes of HYPERKALEMIA?
1. Increased load - Either endogenous from tissue release or exogenous from high intake, which is usually in assoc. with impaired excretion.
2. Decreased excretion - Due to decreased GFR
3. Cellular redistribution - shifting of intracellular space (major site of K) to excellular space.
4. Pseudohyperkalemia: R/T improper collection or transport of blood sample.
RFs of HYPERKALEMIA
Impaired renal excretion of K
Massive cell breakdown (Rhabdo, burns, trauma)
use of K-sparing diuretics
Excess K supplementation
HYPERKALEMIA - Etiology
Traumatic venipuncture or fist clenching during blood stick.
Impaired K excretion
Medication induced (long list!) p. 602
History of HYPERKALEMIA
PE of HYPERKALEMIA
Decreased deep tendon reflexes
Flaccid paralysis of extremities
Initial LABS/TEST of HYPERKALEMIA
UA, K, creatinine, osmoles (to calculate fractional excretion of K and transtubular K gradient)
EKG: likely to see peaked T-wave in precocial leads (most common usually earliest EKG change)
Sine wave at very high K
Medication for HYPERKALEMIA
Calcium Gluconate IV to stabilize myocardial membranes.
Kayezalate 30-60 g PO (will cause a sodium load so be careful in cardiac or renal failure.
HYPOKALEMIA - Defined
Serum potassium less than <3.5 mEq/L
RFs of HYPOKALEMIA
Familiar Hypokalemia periodic paralysis --> Hypokalemia after a high-carb or high-NA meal or after excretes.
Congenital adrenogenital syndromes
Liddle syndrome: increased K+ secretion
Familiar interstitial nephritis
General prevention for HYPOKALEMIA
When initiating a diuretic, especially a loop and thiazide diuretic, advise patients to increase their dietary K+ intake.
Etiology of HYPOKALEMIA
Most common causes:
Decreased Intake - alcoholism, elderly, anorexia
GI loss - Vomiting/diarrhea, NG tube, laxative abuse, fistulas, villous adenoma, ureterosigmoidostomy, malabsorption.
Intracellular shift of K
Renal potassium loss (due to drugs, CHF, MH crisis, mineralocorticoid-excess states).
History of HYPOKALEMIA
PE of HYPOKALEMIA
Disorders that may alter lab results: Leukemia and other conditions with high WBCs
BMP, urinary K+, ECG
TREATMENT - HYPOKALEMIA
Nonemergent -- >2.5 mEq/L and no cardiac symptoms --> Oral therapy is preferred 40-120mEq/day in divided dosages
What is the role of the thyroid gland?
Production of T3 and T4. TSH starts in the pituitary gland.
What is the role of the parathyroid gland?
Controls the amount of Calcium in the blood and within the blood.
High TSH indicates what?
Failure of the thyroid to produce sufficient hormone.
Low TSH indicates what?
Too much TSH production.
What level is typically elevated in pregnancy?
T4 due to an increase in the amount of circulating estrogen.
Use of estrogen or HRT can also increase T4 levels.
HYPOTHYROIDISM - defined
Resulting from decreased circulating levels of free thyroid hormone or from resistance to hormone action.
What is subclinical hypothyroidism?
TSH of >4.5 with normal free T4
RFs of hypothyroidism?
Personal/family HX of autoimmune disorders
DM Type I or addisons
Previous postpartum thyroiditis
Previous head/neck irradiation
HX of Graves
Treatment with Lithium, immune modulators or iodine-containing anti arrhythmic amiodarone.
More common in Japanese decent.
Etiology - HYPOTHYROIDISM
Following Iodine Therapy or thyroid surgery.
May result of autoimmune thyroiditis or idiopathic
May also occur with goiter such as hashimoto thyroiditis.
Iodine Deficiency (rare)
May be due to lack of TRH from hypothalamus or TSH from pituitary.
Transient - silent from postpartum.
History of HYPOTHYROIDISM
Onset may be insidious
Weakness, fatigue, lethargy
Decreased memory, concentration
Modest weight gain
PE of HYPOTHYROIDISM
Dry coarse skin
Dull facial expression
Coarsening or huskiness to voice
Swelling or hands/feet
Reduced systolic BP
Increased diastolic BP
Reduced body and scalp hair
Delayed relaxation of deep-tendon reflexes
Labs/Testing of HYPOTHYROID
Primary -- TSH and Free T4
Medications - HYPOTHYROID
Levothyroxine - 1.6mcg/kg/d and increase by 25 mug every 4-6 weeks until TSH is within normal range.
What dosage should you start with in elderly for hypothyroidism?
25mcg of Levothyroxine
HYPERTHYROID (Thyrotoxicosis) - Defined
Thyroid hormone excess
Most common form of hyperthyroidism.
Diffuse goiter and thyrotoxicosis is common.
What is the patho Graves Disease?
Characterized by auto reactive agonistic antibodies to the TSH receptor.
Toxic Multinodular Goiter
2nd most common.
TSH receptor mutation has been found in 60% of pt's.
TSH over 10 indicates?
Indicates clinical hypothyroidism AND
abnormal lipid panels!
Treatment of the TSH may help the lipids and therefore decreasing cardiac risk.
TSH between 5-10
Subclinical - Recheck in 30-60 days
When should subclinical hypothyroid be considered to treat?
Presence of thyroid antibodies
Symptoms of hypothyroidism
Personal or family HX of autoimmune thyroid disease
The presence of hyperlipidemia, cardiac dysfunction, or risk of CV disease.
Menstrual disturbances and desire for pregnancy
What is the most common etiology of hypothyroid in the US?
Hashimotos Autoimmune Thyroiditis
What are the iatrogenic causes of hypothyroid?
Amiodarone --> contains iodine
Dopamine and lithium --> Affects hypothalamic-pituitary axis and release of TRH and TSH.
Pituitary Tumur --> causes central hypothyroidism
What is thyroid storm?
A severe sometimes fatal form of HYPERthyroidism.
Initial symptoms are fever, nausea, vomiting, abdominal pain.
Progressive symptoms are severe agitation, psychosis, fever, diaphoresis, tachycardia, heart failure, atrial fibrillation, or atrial flutter, confusion, cardiovascular collapse.