HTHSCI 3PF1 Final Exam

What are the acute complications of diabetes?

Hypoglycemia and hyperglycemic states of diabetic ketoacidosis and hyperosmolar hyperglycemic nonketotic syndrome

what are the triggers for acute complications of diabetes?

concurrent illness and factors related to the management of plasma glucose levels including noncompliance with diet or pharmacological therapy or side effects of pharmacological therapy

chronic complications of DM

macrovascular and microvascular

Microvascular complications

retinopathy, nephropathy, neuropathy

Macrovascular complications

Cerebrovascular disease

PVD

CAD

Chronic hyperglycemia and resultant metabolic events have been associated with

chronic complications

Hyperglycemia affects cells that do not effectively reduce the transport of glucose into the cell in a hyperglycemic state results in

intracellular hyperglycemia

Cells that are vulnerable to hyperglycemia

capillary endothelial cells in the retina

mesangial cells in the renal glomerulus

neurons and schwann cells in peripheral nerves

the hemostatic mechanisms of the body generally maintain glucose at

< 6.0 mmol/L

what source of energy does the brain solely rely on?

glucose

Hypoglycemia causes the development of

neurogenic/autonomic and/or neuroglycopenic symptoms

Hypoglycemic activation of the SNS results in what symptoms?

neurogenic or autonomic symptoms of trembling, palpitations, sweating anxiety, hunger, nausea, and tingling

Abrupt cessation of glucose delivery to the brain results in what type of symptoms?

neuroglycopenic symptoms: difficulty concentrating, weakness, drowsiness, vision changes, headache, dizziness, and difficulty speaking

Symptoms are variable among ___________ and ____________, however they are usually __________ for each person

children, elderly, consistent

Hypoglycemia is ______ than normal glucose levels

lower (2.5-3.3 mmol/L)

What is considered hypoglycemia in diabetic patients treated with insulin or insulin secretagogues?

BG levels < 4mmol/L

Symptoms of hypoglycemia respond to the administration of what?

carbohydrates

Hypoglycemia may be caused by what mechanisms?

Exogenous, endogenous, or functional

What is the most common cause of hypoglycemia?

endogenous mechanism of drug induced hypoglycemia

Endogenous mechanism (drugs) of hypoglycemia may make patients reluctant to intensify what?

pharmacological therapy

Short term risks for hypoglycemia

It would be unsafe if an individual experiencing hypoglycemia was driving or operating heavy machinery --> risk of coma

What symptoms are prolonged comas associated with?

transient neurological symptoms like, paresis, convulsions, and encephalopathy

the long term risks of hypoglycemia

mild intellectual impairment and rarely permanent neurologic sequelae like hemiparesis and pontine dysfunction

Mild hypoglycemia

autonomic symptoms, able to self-treat

moderate hypoglycemia

autonomic and neuroglycopenic symptoms, able to self-treat

Severe hypoglycemia

unable to self-treat, requires assistance, unconsciousness may occur

BG of severe hypoglycemia

usually <2.8 mmol/L

what are the two-fold causes of hypoglycemia?

1. excess of insulin may be a result of too much exogenous insulin or insulin secretagogues

2. deficits in glucose counterregulation

Who is hypoglycemia more common in? %?

Type 1 diabetics and occurs in more than 90% of type 1 diabetics and often limits the management of the disease

Can hypoglycemia occur in T2DM, how?

yes, particularly in those taking insulin secretagogues or insulin

What type of diabetes is glucose counterregulation deficits most important in?

type 1

What happens with recurrent episodes of hypoglycemia? Glucose counterregulation deficits

glucagon and epinephrine release during hypoglycemia become defective, which blunts the autonomic symptoms associated with mild and moderate hypoglycemia and puts these patients at greater risk of severe hypoglycemia

Risk factors for deficits in glucose counterregulation

exercise, alcohol, older age, renal dysfunction, infection, error in insulin dose, medication changes cognitive dysfunction, mental health issues

Specific risk factors for severe hypoglycemia in type 1 DM

prior episode of severe hypoglycemia, current low A1C <6%, hypoglycemia unawareness, long duration of diabetes, autonomic neuropathy, low economic status, adolescence, preschool children unable to detect and treat on their own

What is the first line of defence against hypoglycemia?

a decrease in endogenous insulin secretion

Decrease in endogenous insulin is critical in patients who have what?

residual insulin secretion

When do beta cells normally suppress insulin secretion at?

4.6 mmol/L

Counterregulatory mechanism of hypoglycemia

Hypoglycemia activates SNS via hypothalamus which results in stimulation of the adrenal gland to release counterregulatory hormones

What is the role of the liver in sympathoadrenal response to hypoglycemia?

two-fold

Liver in response to hypoglycemia

The portal vein may play a role in sensing hypoglycemia and activating the counterregulatory response:

glucagon stimulates glycogenolysis and gluconeogenesis in the liver

Role of counterregulatory hormones

norepinephrine, epinephrine, GH, and cortisol cause increase in glucose production, and decrease uptake in the periphery specifically adipose and muscle tissue

When do neuroglycopenic symptoms occur?

due to an abrupt cessation of glucose delivery to the brain

How is mild to moderate hypoglycemia treated?

15g carbohydrate → increase in 2.1 mmol/L in 20 mins

Severe hypo but conscious person treatment

20g carbohydrate → 3.6 mmol/L increase at 45 mins

When should you retest BG in both severe and mild-mod hypoglycemia?

in both severe and mild-mod hypoglycemia, patients should re-test BG in 15 minutes and retreat with 15 or 20g of carbohydrate if BG < 4 mmol/L

Treatment in unconscious person with severe hypoglycemia > equal to 5 years of age

1mg glucose SC or IM OR IV glucose 10-25g ( 20-50 cc D50W) over 1-3 mins

examples of 15g carbohydrates

glucose tabs, 3 tspns or 3 packs of table sugar dissolved in water, 175 mL juice or soft drink, 6 life savers, 1 tablespoon honey

What type of sugar is preferred when treating hypoglycemia?

monosaccharides like glucose are preferred as they are absorbed directly into bloodstream

consideration for hypoglycemic pts taking alpha-glucosidase inhibitor

dextrose not sucrose should be used to treat hypoglycemia

When will glucagon be ineffective?

in patients whose glycogen stores are depleted

When will glucagon not be as effective?

in individuals who have consumed more than 2 standard alcoholic drinks within the previous few hours or those who have advanced liver disease

Why are hyperglycemic emergencies important?

they are life-threatening and associated with morbidity and mortality

both DKA and HNNK are conditions that arise from either a what?

relative or absolute insulin deficiency

trigger for hyperglycemic emergencies

increase in counterregulatory hormones and resultant hyperglycemia

Notes about HHNKS

Osmotic diuresis and extracellular fluid volume depletion or hypovolemia is more impressive with HHNKS and acid-base imbalance specifically metabolic acidosis due to ketoacidosis is less likely to occur in HHNKS but always present in DKA

________ ___________ occur due to metabolic acidosis and osmotic diuresis

electrolyte imbalances

The most serious electrolyte imbalance is ____ and _____________ due to associated risk for ________ ___________

hypo and hyperkalemia, cardiac arrhythmias

An adverse neurological sequelae including ________ _______, _____ and ________ are reported in DKA and HHNKS

cerebral edema, coma, death

the pathophys of HHNKS/DKA is an ______ ______ and some precipitating factor that _______ _________________ hormones including __________

insulin deficiency, increases counterregulatory, glucagon

___________ directly stimulates _______________ in the liver

glucagon, glycogenolysis

________________ hormones including ___________ cause _____________ glucose __________ in the peripheral tissues

counterregulatory, glucagon, decreased, uptake

_________ breaks down to provide amino acids to the liver for _________________

protein, gluconeogenesis

_________ ________ also breaks down to form __________ for gluconeogenesis if there is a ________ insulin deficiency and _____ ______ ______ to form _______ in the liver in the case of _______ insulin deficiency

adipose tissue, glycerol, relative, free fatty acids, ketones, absolute

Specific _________ formed are called ____-______________ and ______________ acids which result in _____________ _________

ketones, beta-hydroxybutyric, acetoacetic, metabolic acidosis

The result of ___________ and _____________ is hyperglycemia

glycogenolysis, gluconeogenesis

Hyperglycemia causes ________ _________ and large losses of ______________ in the urine

osmotic diuresis, electrolytes

The total body deficit of water in adults is usually about ____ L in ________ and _____ in ______ which represents a loss between _______% of body weight

5-7L, DKA, 7-12 L, HHNKS, 10-15%

If left untreated __________ _______ ensues

circulatory failure

________________ and ____________ __________ can both cause ___ ______________ and if left untreated _____

hyperosmolality, metabolic acidosis, CNS depression, coma

Whether the hyperglycemia is classified as DKA or HHNKS depends on whether or not there is ___________ or ____________ insulin deficiency

relative or absolute

T/F DKA is more common than HHNKS

true

1 multiple choice option

Between _____-________ patients are admitted to hospital every year because of DKA

5000-10,000

3 multiple choice options

T/F mortality is lower with DKA compared to HHNKS

true

1 multiple choice option

mortality of DKA

4-10%

DKA glucose

>14 mmol/L

Extracellular _____ ______ __________ and ______________ ____________ common in both DKA and HHNKS

fluid volume depletion, electrolyte imbalances

________ ___________ is present with a pH of less than or equal ____ and decreased ____________

metabolic acidosis, 7.3, bicarbonate

Bicarbonate levels of DKA resulting in metabolic acidosis

15 mmol/L or less

DKA results in Ketone production → presence of typical ________ ______ (_______)

acetone breath, fruity

DKA results in ____________-_______ respirations due to _________ metabolic acidosis

Kussmaul-kein, severe

_________ patients admitted with HHNKS to hospital per year

500-1000

3 multiple choice options

T/F HHNKS has a higher mortality rate compared to DKA

true

1 multiple choice option

how many die from HHNKS?

10-50%

why is the mortality rate high with HHNKS?

Likely due to underlying illnesses

Plasma glucose much ________ in HHNKS (____ mmol/L)

higher, >34

________ depletion is greater in __________

ECFV, HHNKS

Plasma glucose levels are _______ in HHNKS resulting in ________ ________ ___________

higher, greater osmotic diuresis

Osmolality in HHNKS ___ mOsm/L

>320

__ is usually ______ in HHNKS

pH, normal

T/F: in HHNKS, Acetone breath and kussmaul-kien respirations usually present

false

1 multiple choice option

_____________ and ____________ may be present in either DKA or HHNKS due to _______ _________

hypotension, tachycardia, ECFV depletion

_______ __________ is used in DKA and HHNKS to restore normal _____ and _______ ____________

fluid rehydration, ECFV, tissue perfusion

Correction of _____________ by addressing ________ or _________ _________ ________________

hyperglycemia, absolute, relative insulin deficiency

Resolution of ___________ usually occurs with _________ therapy and ______ ______________

ketoacidosis, insulin, rehydration

For severe acidosis ______ ______________ may be used in the adult population

sodium bicarbonate

T/F sodium bicarbonate is usually used in the paediatric population for severe acidosis

false

1 multiple choice option

what electrolyte do we specifically need to monitor for HHNKS/DKA?

potassium

Monitor for and prevent complications specifically adverse _____________ __________ like _________ ________

neurological sequelae, cerebral edema

_______________ is added to maintenance fluid even if __________ levels are not abnormally _______ because when ___________ _________ begins to correct _____________ shifts back into the cell

potassium, potassium, low, metabolic acidosis, potassium

Since there is already an overall ______________ of _____________ due to potassium having moved out of the cell during ________ ________ and loss of potassium via ___________ _________ it is imperative to anticipate this to avoid life-threatening ________________

depletion, potassium, metabolic acidosis, osmotic diuresis, arrhythmias