Symptom: Polydipsia

Sepsis causes hypoglycemia how

Cytokine accelerated glucose utilization, inhibition of gluconeogenesis, glycogen depletion

Test patients with recurrent candidal vaginitis and poor wound healing for

DM

Canagliflozin, Dapagliflozin, Empagliflozin

Decrease glucose absorption Adverse Effects: Glucosuria (UTI, candidiasis), dehydration, hyperkalemia, weight loss

Acarabose

Decrease glucose absorption Adverse effects: GI upset

What physical exam findings could suggest peripheral vascular disease?

Decreased peripheral pulses and bruits

What blood sugar targets are reccomended to reduce risk of macrosomia?

Fasting or preprandial blood glucose <95 Postprandial blood glucose <140 at 1 hour, <120 at 2 hours

If diabetes remains uncontrolled for a long time, what micro and macro vascular complications could occur?

Micro: neuropathy (peripheral and autonomic), nephropathy, retinopathy Macro: angina/MI (CAD), claudication (periph. vascular disease), TIA/stroke

Gestational Diabetes Mellitus (GDM)

any degree of glucose intolerance with onset or first recognition during pregnancy increase secretion of fetoplacental hormones-->increasing insulin resistance, B cell function is insufficient to overcome the insulin resistance

Autonomic Neuropathy

damage to nerves supplying the internal body structures that regulate functions such as blood pressure, heart rate, bowel and bladder emptying, and digestion

ABI (ankle brachial index)

evaluates circulation in legs; doctor listen to flow of blood and measures blood pressure in both arms and feet; normally should be equal; significant difference indicates lack of blood flow =(pressure in R foot)/highest pressure of arms >.9= normal .4-.9= mild-moderate PAD <.4= severe PAD

Why does the body need to undergo gluconeogensis if it spends time breaking down glucose?

key organs (brain) use glucose as an energy source primarily. It is vital to maintain a minimum blood glucose concentration

Macrosomia

large-bodied baby commonly seen in diabetic pregnancies

Somatostatinoma

malignant pancreatic islet tumor -> diabetes mellitus

Non proliferative Retinopathy

most common form of retinopathy; first visible changes seen in the retina: micro-aneurysm, hemorrhage, cotton wool spots "proliferative" refers to whether or not there is neovascularization (abnormal blood vessel growth) in the retina

hypernatremia

sodium over 145 (over 158 if severe) -due to water loss, all hypertonic (high sodium=low water)

SIADH

syndrome of inappropriate antidiuretic hormone high ADH-->increased water retention--> decreased aldosterone-->increased urine sodium excretion dilute plasma, concentrated urine

Hyperinsulinism

the condition of excessive secretion of insulin in the bloodstream, causes hypoglycemia

Osmotic Demyelination Syndrome

what occurs when you correct hyponatremia too fast Areas in the pons indicate massive demyelination of descending axons

Hypoglycemia

Blood glucose less than 70 Sx: TIRED Tachycardia Irritability Restless Excessive Hunger Diaphoresis

hypotonic hyponatremia

Can be hypovolemic, euvolemic, or hypervolemic Serum osmolality is low (below 280), along with low sodium

What type of skin infection is common in skin folds of patients with DM? Why?

Candida (identify due to classic satellite lesions) Fungus love glucose

Why check for carotid bruit's in patients with DM? Why do a foot exam?

Check for carotid bruits because the patient is at risk for stroke Foot exam is important because patients often have ulcers but cannot feel them because peripheral neuropathy

What would you find in a patient with mild to moderate peripheral artery disease (PAD)?

Claudication (pain/cramping while walking)

Primary/Psychogenic Polydipsia

Compulsive drinking of water that is associated with a psychiatric illness such as psychosis or OCD Water Deprivation Test is used to distinguish between this and other causes of polydipsia

Dexcom is used for

Continuous glucose monitoring (CGM)

What is the general principle for safely correctly hyponatremia?

Correct osmolality of plasma at a rate that reflects the rate of creation of hyponatremia

How does a pre-diabetic decrease his/her risk?

-Lose 7% of body weight -moderate exercise (brisk walking) for 30 minutes, 5 times a week (150 mins per week) -resistance training 2-3x per week

Nephropathy Treatment

-Strict glycemic control (A1C<7%) -Control blood pressure -ACE inhibitors and ARBs (angiotensin receptor blockers) to inhibit Renin angiotensin aldosterone system

What happens to brain volume during hyponatremia?

1. In acute hyponatremia, the low levels of sodium cause water to move into the brain. 2. The brain produces more electrolytes (Na+ and K+) which leave the brain. 3. Water moves out of the brain along with the electrolytes.

What are the 2 causes of the defect in renal water excretion that leads to hyponatremia?

1. Low effective circulating volume-->limits volume of dilute urine delivered to distal diluting sites 2. Elevated ADH causes reabsorption of the dilute urine (this was on Dr. R's slides and I have no idea what it means)

Type 2 DM is characterized by what 3 underlying pathophysiological defects?

1. Peripheral insulin resistance 2. Impaired regulation of hepatic gluconeogenesis 3. Impairment of beta cell function (fail to compensate for insulin resistance, function declines with increasing glucose levels)

What are the 3 P's of Diabetes?

1. PolyUREA= Much urination 2. PolyDipsea= Much thirst 3. PolyPHAGIA= Much eating

Potassium levels may be high, low, or normal despite total body potassium is depleted in HHS and DKA. If labs reveal hyperkalemia, overall potassium may be low due to what 2 things?

1. Transcellular shift with acidosis (acidosis causes K to move out of the cell) 2. Loss of potassium through urine due to osmoatic diuresis

What is normal plasma osmolality

280-300 mOsm/L

Hyponatremia

A serum sodium level less than 135 mEq/L. Common cause: Solute loss due to diarrhea, vomiting, renal losses, etc-->water retention by drinking water alone-->water in excess of solutes-->hyponatremia A water problem, not a sodium problem

What are the end products of ketogenesis?

Acetone and 3-hydroxybutyrate

When should a pregnant woman be screened for gestational DM?

After 24 weeks of gestation (~6 months)

At what age should patients be screened for diabetes?

All patients starting at age 45, at any age if BMI>25

What is the difference betwen dehydration and volume depletion?

Dehydration:free water defecit-->hypernatremia Treatment: free water repletion slowly Volume depletion: extracellular fluid or effective circulating blood volume depletion Treatment: isotonic fluid replacement (more rapidly) Correct volume deficits first, then correct water imbalance slowly

Nonenzymatic glycation and glyco-oxidation is a chronic complication of _______ which can lead to

Diabetes Mellitus, peripheral neuropathy and autonomic neuropathy

Cotton wool patches are commonly found in patients with ______. What are they?

Diabetes patiens due to ischemia and nerve damage

Cataracts are commonly found in patients with ____. What are they?

Diabetes, due to sorbitol accumulation in lens and apoptosis of lens

Hypertonic Hyponatremia

Due to osmotic shift (hyperglycemia) Add 1.6 to Na for every 100 increase in glucose over 100 Ex: Na 129, Glucose 500 500-100=400, 4x1.6=6.4, 129+6.4=135 which is normal

proliferative Retinopathy

END STAGE angiogenesis due to hypoxia that stimulates the production of angiogenic factors (including VEGF)

Nephrogenic Diabetes Insipidus Etiology Findings Water Deprivation Test Treatment

Etiology: Hereditary (ADH receptor mutation), hypercalcemia, hypokalemia, lithium, demeclocycline (ADH antagonist) Findings: normal to increased ADH Water Deprivation Test: minimal change in urine osmolality even after administration of ADH analog Treatment: HCTZ (HCTZ is a thiazide diuretic--blocks Na reabsorption in the DCT so both Na and H2O are lost in the urine which causes mild volume depletion-->nephron reacts by reabsorbing Na and H2O proximally)

Central Diabetes Insipidus Etiology Findings Water Deprivation Test Treatment

Etiology: pituitary or hypothalamus pathology Findings: low ADH Water Deprivation Test: >50% increase in urine osmolality only after administration of ADH analog Treatment: Desmopressin (synthetic ADH), Hydration

Liver failure can cause hypoglycemia how

Gluconeogensis and glycogenolysis are impaired

What should be checked every 6 months in a patient with DM?

Hgb A1c every 6 months (every 3 months if uncontrolled DM or new changes to meds)

What are the hyperglycemia and hypoglycemia symptoms of diabetes mellitus?

Hyper: 3p's (polydipsia, polyuria, polyphagia), weight loss, fatigue, fungal infections Hypo: sweaty, tremors, palpitations, drowsy/coma, stroke like, seizures

Classic New Onset Type 1 DM presentation

Hyperglycemia, without acidosis is most common

Hyperosmolar (hypertonic) hyponatremia

Hyponatremia with measured serum osmolality > 300mOsm -excessive glucose creates a hypertonic, hyperosmolar extracellular fluid. Water goes out of the cells into the extracellular fluid and dilutes sodium Result: dilution of sodium with hyponatremia

Summarize hyponatremia and hypernatremia

Hyponatremia=too much water main treatment is water restriction (but depends on volume status) Hypernatremia=water loss main treatment is free water (D5W)

How do you treat hyponatremia--hypovolemic, euvolemic, and hypervolemic?

Hypovolemic: Isotonic saline Euvolemic: Water restriction Hypervolemic: NA and Water restriction

How does weight loss and exercise help a type 2 DM patient?

Improves insulin sensitivity

diabetes insipidus

Inability to concentrate urine due to either lack of ADH (central) or failure to response to ADH (nephrogenic) Sx: polyuria, high serum osmolality, hypernatremia, low urine osmolality, low ruine specific gravity concentrated serum, dilute urine

Linagliptin, Saxagliptin, Sitagliptin

Increase glucose-induced insuline secretion Adverse effects: Respiratory and urinary infections, increase satiety (no weight changes)

Glipizide and Glyburide (sulfonylurea class)

Increase insulin SECRETION Adverse effects: weight gain and hypoglycemia

Pioglitazone and rosiglitazone

Increase insulin sensitivity Adverse effects: weight gain, edema, heart failure Rosiglitazone: increased risk of myocardial infarction (don't give to patients with CAD)

What physical exam findings could suggest coronary artery disease?

Increased JVP, fourth heart sound, displaced PMI (point of maximar impulse)

Exanatide and Liraglutide

Increased glucose-induced insulin section Adverse reactions: N/V, pancreatitis, weight loss

metformin

Increases insulin sensitivity Adverse effects: Vitamin B12 deficiency

What antibody is made against pancreatic beta cells in type 1 DM? Which HLA molecules is type 1 DM associated with?

anti-GAD (glutamic acid decarboxylase) HLA DR3/DR4 HLA-DR4 and DR3 (4-3=1)

Type 1.5 Diabetes

Islet antibodies are present (as in type 1) but the progression of B cell failure is very slow

What does the nitroprusside reaction measure? For what types of patients?

It is used to measure acetoacetate and acetone levels in serum and urine, but NOT hydroxybetabutyrate, so it may under estimate the degree of ketonemia and ketonuria Used commonly for DKA patients, if available use a serum hydroxybetabutyrate test

What is the HbA1C goal in a diabetic patient?

Less than 7%

What does insulin do in liver, muscle, fat, and cell membranes?

Liver: increase glucose storage as glycogen Muscle: increase glycogen and protein synthesis Fat: increase triglyceride storage Cell membrane: increase potassium uptake

Distal symmetric polyneuropathy

Most common form Affects hands and/or feet bilaterally "stocking and glove distribution" Loss of sensation, abnormal sensations, pain, and paresthesias

Acute Hyponatremia Symptoms

Nausea, malaise, stupor, coma, seizures

Water Deprivation Test

No water intake for 2-3 hours followed by hourly measurments of urine volume and osmolarity and plasma Na concentration and osmolarity. ADH analog (desmopressin acetate) is administered if normal values are not reached used to differenciate between central and nephrogenic DI

Silent asymptomatic discovery of Type 1 DM

Normogylcemic individuals who develop two or more type 1 DM associated islet antibodies (ex: Ab to insulin, GAD65, ZnT8)

What is the limit of using Hypertonic Saline to treat hyponatremia?

Overcorrection can cause osmotic demyelination

Pseudohyponatremia (isotonic)

Patient with hyponatremia, but normal plasma osmolality examples: -hyperlipidemia or hyperproteinemia (MS) increase plasma osmolality (proteins or lipids (INSOLUBLE) are just taking up a greater percentage of blood volume, making sodium look low) The major solutes contributing to serum osmolality in mammals are sodium (Na+), potassium (K+), chloride (Cl−), bicarbonate (HCO3−), blood urea nitrogen (BUN), and glucose (Glu) but any solute in the plasma contributes

What is the diagnostic criteria for nephropathy?

Positive 2 out of 3 for micro albuminuria over a 6 month period (24 hour urine collection--spot albumin/Cr ratio)

Monofilament test

Predicts the risk of future for ulcers in the foot. Use in patients with diabetic neuropathy.

Dehydration assessment

Progression: Decreased skin turgor--> Orthostatic change in pulse--> Orthostatic change in pulse and BP--> Supine hypotension

What are the different types of Insulin medications?

Rapid: Lispro, Aspart, Glulisine (LAG) Short Acting: Regular Intermediate: NPH Long acting: Detemir, Glargine

Hyperosmolar Hyperglycemic State (HHS)

Severe dehydration due to hyperglycemic (osmotic) diuresis Classic Patient: old with Type 2 DM with limited ability to drink Insulin present, ketones absent Occurs when there is enough insulin to prevent ketosis, but not enough to suppress hyperglycemia. Since no acidosis symptoms are present, patients often endure a longer period of osmotic dehydration before presentation (hence plasma glucose >600) Profound hyperglycemia-->excessive osmotic diuresis-->dehydration and increased serum osmlality-->HHS

HHS (hyperosmolar hyperglycemic state) triad

Severe hyerglycemia, undetectable ketones with absence of acidosis, plasma osmolality greater than 340

Diabetic Ketoacidosis (DKA)

Severe insulin deficiency leading to severe hyperglycemia and ketogenesis Insulin absent, ketones present DKA is Deadly: Delirium/psychosis, Kussmual respirations, Abdominal pain/nausea/vomiting, Dehydration Fruity Breath Odor due to exhaled acetone Insulin noncompliance or increased requirements from increased stress-->excess fat breakdown and ketogenesis from free fatty acids-->ketone bodies

What is essential if micro albuminuria (30-300mg) is present in a patient with nephropahy?

Strict glycemic control to limit progression to macro albuminuria (>300mg) and to end stage renal disease

Hyponatremia with low plasma osmolality

TRUE hyponatremia

When should a DM patient be screened for diabetic retinopathy?

Type 1: after 5 years of diagnosis Type 2: at the time of diagnosis

When should a DM patient be screened for nephropathy? What is the gold standard?

Type 1: after 5 years of diagnosis Type 2: at the time of diagnosis Then annually Gold Standard: 24 hour urine collection

What is the DKA triad?

Uncontrolled hyperglycemia, increased total body ketone, metabolic acidosis (anion gap)

Insulinoma

a benign tumor of the pancreas that causes hypoglycemia by secreting additional insulin

Nephropathy

a disease of the kidneys caused by damage to the small blood vessels or to the nephrons Nodular glomerular sclerosis due to hyaline deposits in the kidney called Kimmelstiel-Wilson Nodules Kidney stops working and dumps protein in the urine..check for ANY albumin in the urine, BUN, and Creatinine

Cerebral Salt Wasting

a potential cause of hyponatremia in a patient with a CNS disease. Cerebral salt wasting is characterized by hyponatremia with elevated urine sodium and hypovolemia (CNS disease=BNP release/decreased sympathetic activity-->decreased Na+ reabsorption and volume depletion)