Pathophysiology Final exam

started at diabetes on study guide

Type 2 Diabetes

• initially higher blood glucose levels lead to higher insulin production, leading to desensitization of cells to insulin, increasingly higher insulin production, and beta cell exhaustion with the loss of ability to produce insulin

risk factors for Type 2 diabetes

• often can affect fat based on where fat is at

• advancing age

• obesity

• family history of DM

• history of gestational diabetes

• impaired glucose matabolism

• physical inactivity

treatment for type 2 diabetes

• usually managed initially with oral antidiabetic medications (often metformin, then a GLP-1 antagonist) that increase insulin production and action

• as the condition progresses, supplemental insulin is often necessary as pancreatic production declines

gestational diabetes

• a form of glucose intolerance that is diagnosed during

  pregnancy that is associated with increased risk of developing type II diabetes- normal to have a slight increase to have some extra for the fetus but if above around 95 then warning sign of significant insulin resistance

• can increase risk of hypertension of preeclampsia in moms

treatment for gestational diabetes

• treatment usually includes lifestyle changes and insulin

• insulin doesnt cross placenta

• about 5-10% of women will be diagnosed with type 2 diabetes immediately following preganancy

• women who have had gestional diabetes have a 40-60% chance of developing diabetes w/in 5-10 years

general symptoms of diabetes

• hyperglycemia- high blood sugar b/c sugar staying in cells

• Glucosuria- so much glucose n it oversaturated kidneys ability to break it down it can leak into urine, water moving to sugar

• polyuria(a lot of urine,losing hella water,), polydipsia(drinking a lotof water)

• polyphagia(can mean hunger, have lots of glucose in body but body cant use it)

• weight loss

  • increased breakdown of fat- b/c of less insulin - insulin helps you absorb sugar

  • seen a lot with type 1

• blurred vision

  • excess glucose changes shapes na dflexibility of lens of the eye

• fatigue

diabetic ketoacidosis

• often seen in type 1 diabetes

• sometimes can be first presentation of diabetes

• often an episode is triggered by an infection, pregancy, heart attack, or inadequate insulin administration

• results in hyperglycemia, anion gap metabolic acidosis(cause of acidosis is some extra acidic molecule floating in body- in this case extra ketones), and hyperkalemia(insulin also helps move potassium cells, potassium can get stuck outside in the blood

diabetic ketoacidosis

• often associated with insulin deficiency = breakdown of fats and conversion into ketones, which are acidic

• also accompying this insulin deficiency is hyperglycemia- glucose spills over into urine leading to low blood volume

• symptoms- Kussmaul respirations(rapis deep breathing- response to metabolic acidosis), dehydration, nausea, vomiting, mental status changes

• treatment- fluids, replace electrolytes (K+) if K+ below 5.3 give extra potassium, give insulin

Hyperglycemic hyperosmolar state

• often occurs w/ type 2 diabetes

• if blood sugar is high enough, it causes significant osmotic diuresis(urinate out sugar, and water follows sugar)

• leads to sever dehydration and increased osmolarity of the blood (BP and cardiac functioning)

• treat with fluids, restore electrolyte deficits, repleting insulin, and treating the underlying cause

diabetes chronic complications

• diabetes causes damage to small blood vessels throughout the body

• glucose causes glycosylation of basement membrane in small blood vessels

• small blood vessels thicken and harden leading to ischemia and necrosis

• diabetic retinopathy- blindness

  • diabetes is the leading cause of blindness in the U.S

• diabetic neuropathy

• diabetic nephropathy

  • diabetes #1 cause of renal failure/chronic kidney disease

• amputations

  • poor circulations, ulcers you cant feel

    • about 60% of non-traumatic amputations are due to diabetes

• erectile dysfuction

• pregnancy complications

• metabolic ocncerns

  • hypertension, heart disease, stroke, high cholesterol

  • heart disease #1 cause of death in patients w/ diabetes

how to diagnose and treat diabetes

diagnosis:

• history

• physical examination

• urinanlysis

• fast blood glucose test

• oral glucose tolerance test

• random blood glucose test

• hemoglobin A1C- taking blood cells with different life spans, seeing how much of hemoglobin in blood is glycosolated- 2 month snap shot of how much

• blood pressure measurement and cholesterol

treatment:

• most of these associated with type 2

• dietary changes- lower carb diet

• exercise

• self-glucose monitoring

• weight loss

• oral hyperglycemia medications

• supplemental insulin- primary treatment for type 1

• complication management

how to diagnose diabetes

look at table 10-2 slide

pre diabetes:

• HgbA1c- 5.7-6.4%

• impaired fasting glucose 100-125 mg/dL (fasting pasma glucose)

• impaired glucose tolerance 140-199 mg/dL (2- hour post 75g glucose challenge)

metabolic syndrome

• bunch of conditions that usualy occur together

• hyperglycemia, high BP, hypercholesrolemia, and increased waist circumference (obesity- a lot of stomach fat)

• increases the risk of cardiovascular disease, diabetes, and stroke

• diagnostic criteris include the presence of more than one of those risk factors

• treatment strategies focus on lifestyle changes- losing weight, diet change- things that wont trigger spikes in insulin, physical activity, reducing or stopping smoking

Goiter and Thyroid Nodules

• visibile enlargement of the thyroid glans

• usually painless but may affect the respiratory and gastrointestinal systems

• not necessarily malignant

• can occur in hyperthyroidism(producing extra t3 and t4 that will increase metabolism of other cells), hypothyroidism(producing less of thyroid hormones-these two judge activity not size of thyroid), and normal thyroid states

• iodine deficiency is the most common cause world wide

• a goiter is simply an enlargement of the thyroid- doesn't automatically mean hyperthyroidism

  • it can result from excess TSH stimulating growth, inflammation, or tumors

• Hashimoto’s thyroiditis causes a goiter by hypothyroidism

thyroid goiters classification

nontoxic goiter

• normal levels of TSH, T3, and T4

• iondine deficiency

toxic goiter

• increased thyroid

hypothyroid goiter

• hashimotos thyroiditis

hypothyroidism

• thyroid does not produce sufficient amounts of thyroid hormones

• often due to damage from inflammation

• most commonly caused by autoimmune thyroiditis (hashimotos thyroiditis)

• can also be related to surgery, infections, trauma, or after childbirth

cushing syndrome diagnosis

history, physical examination

Addisons disease symptoms

• most dangerous- hypoaldosteronism (need aldosterone to help you again and absorb salt)

  • hypotension, salt craving

• hypocortisolism

  • hypoglycemia

    • lethargy

    • fatugues and weakness

    • weight loss

  • poor stress tolerance

  • high ACTH

• hyperpigmentation

Addisons disease disagnosis and treatment

diagnosis:

history, physical exam, serum hormone levels (e.g. cortisol, ACTH, and androgens), serum glucose levels, complete blood counts, blood chemistry, adrenal and pituitary CT/MRI, and biopsy

treatment:

lifelong hormone replacement therapy, wear a medical bracelet DIDNT FINISH THIS SLIDEE

blood

consists of

• plasma

• leukocytes- white blood cells

• erythro(blood)cytes- red blood cells

• thrombocytes- platelets

neutrophil

• most common white blood cell

• about 60-70 % of WBCs

• first to arrive on scene jcnjvevajienv

• mainly attack bacteria and fungi

• kill with phagocytosis (eat it, take it in)

eosinophil

• bilobed nucleus

• red colored

• make up around 3% of WBCs

• attacks parasites- main purpose

• granules contain cytotoxic enzymes to attack the parasite

• also involved (can be released) in asthma and allergic reactions

basophil

• bilobed nucleus

• undermicroscope- purple bluish color

• about 1% of WBCs

• granules contain histamine and heparin

• respond to allergens and antigens

monocyte (in blood)/macrophages (anywhere else)

• U or kidney shaped nucleus

• 3-8% of WBCs

• no granules

• professionaln phagocytic cells

• eat bacteria, dead cells and cellular debris

• often clean up crew when damage done to the body

lymphocyte

• lymphoid cells -all come from same stem cell progenators(all others are myeloid progenitor)

• B cells, T cells, and natural killer cells

• about 20% of WBCs

B cells

antibodies!

• initially, B cell only has antibodies covering membrane

• each B cell has a unique antibody that it produces

• since you have so many different B cells, eventually likely there will be one lucky that matches the pathogen (or antigen)

• searching around hoping to be the lucky one

Actiation:

• antigen binds antibody

• brings it into the cell, chops it up, presents it on an MHC II (presents it on a platter to everyone) (MCH- protein cell finger print)

• MCH II binds with a helper T cell receptor that matches