Module 5 Flashcards
Integumentary, Musculoskeletal, Endocrine, and Reproductive
Cause of T1DM?
Autoimmune destruction of insulin-producing beta cells in pancreas
Are T1DM insulin dependent?
Yes
Are T2DM insulin dependent?
No, can be managed by diet and exercise
Symptoms of T1DM
Polydipsia, polyphagia, polyuria
Treatment for T1DM
Insulin therapy, glucose monitoring, healthy diet
Cause of T2DM
Insulin resistance and eventual pancreatic beta cell dysfunction
Risk factors for T2DM
Obesity, sedentary lifestyle, family hx, poor diet
Patho of insulin resistance
Impaired insulin secretion by beta cells and dysregulation of glucose metabolism
Why do T1DM develop DKA?
What glucose level defines DKA?
There is a near total absence of insulin. Glucose cannot enter cells to be used for energy; liver will shift to fat metabolism and ketones accumulate
Glucose > 250
Why do T2DM develop HHNK? What glucose level defines HHNK?
Body still has some insulin but have reduced receptor signaling and increased glucogenesis and impaired glucose uptake by fat and muscle, which leads to accumulation.
Glucose > 600
What does the lack of insulin cause in T1DM?
Ketoacidosis: retinopathy, nephropathy, neuropathy, and cardiovascular diseases
What does the lack of insulin cause in T2DM?
HHNK: same complications as DKA; damage in the pancreas, blood vessels, and nerves. Has FFAs, cardiac dysfunction, lipotoxic cardiomyopathy, and reduced insulin sensitivity in skeletal muscle
Causes of PCOS
Insulin resistance in indicated which cause ovaries to produce androgens; low progesterone, genetics, poor diet, sedentary lifestyle, stress
Comorbidities associated with PCOS
Infertility, obesity, T2DM, dyslipidemia, HTN, atherosclerosis, anx/dep, chronic inflammation
What is the definition and cause of primary amenorrhea?
Menstruation not beginning by age 16
Genetic/anatomic abnormalities, pituitary hypothalamus/ovarian disorders, Turner’s syndrome, sudden weight loss
What is the definition and what are secondary causes of amenorrhea?
Absence of menses for > 3 months in females who has a regular cycle; or > 6 months for females with irregular cycles
Usual cause is pregnancy; can be stress, weight loss, ovarian disorders (tumors, primary ovarian failure), PCOS
Complications associated with metabolic syndome
Increased risk of T2DM, cardiovascular disease, MASLD, MASH, MI, stroke, kidney dysfunction
Labs associated with metabolic syndrome
↓ HDL, ↑ LDL, ↑ triglycerides
What is the role of insulin in metabolic syndrome?
Reduces glucose uptake by cells despite high insulin levels, leading to hyperglycemia and hyperinsulinemia
Greenstick fracture
Incomplete; bone is bent and only outer curve of bend is broken
Simple fracture
Single break in bone, keeps alignment
Transverse fracture
straight across bone shaft
Oblique fracture
at an angle to bone shaft
Spiral fracture
twists around bone shaft
Communited fracture
multiple fracture lines and bone pieces
Compression fracture
bone is crushed or collapsed
Telescopic fracture
one fragment of bone slides over the other, caused by significant source that drives two ends into each other.
common in older adults, requires surgery
Buckle (torus) fracture
Incomplete fracture where one side of bone compresses and buckles but other side is intact; caused by axial loading or compression (falling on outstretched hand)
Common in children with soft bones
Compound fracture
open fracture, goes through skin
What is the role of osteoclasts?
(catastrophic)
resorbs, breaks down bone
What is the role of osteoblasts?
(build)
reabsorbs; builds the bone and secretes COLLAGEN and ground substances to form non-MINERAL bone matrix
First stage of bone healing/remodeling
Inflammatory/Reactive Phase
1-7 days post-injury
Hematoma formation; cytokines and immune cells clean up debris
Second Stage(s) of bone healing/remodeling
1st Reparative
7-21 days post-injury
Soft callus formation; angiogenesis for nutrient supply
2nd Reparative
2-6 weeks post-injury
Hard callus formation; site gains stability
Third Stage of bone healing/remodeling
Month to years post-injury
Formation of mature bone or ossification; bone is now lamellar
Osteoclasts resorb excess bone, osteoblasts form new bone
Risk factors for osteoporosis
Elderly, female, post-menopausal, small bone, fair skin, light hair/eyes, Ca/Vit D deficiency, smoking, caffiene, meds (GLUCOCORTICOID, ANTICONVULSANTS, PPIs, SSRIs, chemotherapeutics, loop diuretics)
Causes of osteoporosis
RANK-RANKL is normal process of breaking down and rebuilding bone; OPG prevents RANK-RANKL by enhancing osteoclast activity
Definition of osteoporosis
Metabolic bone disorder is characterized by bone density and strength
Complications of osteoporosis
Loss of height, kyphosis, chronic pain/inflammation, increased risk of fractures
Normal DEXA scan
> -1.0
DEXA scan for osteopenia
-1.0 and -2.5
DEXA scan for osteoporosis
< -2.5
Primary cause of gout
MONOSODIUM URATE crystal deposition in joints (hyperuricemia)
Uric acid > 6.8
Risk factors of gout
Men, high intake of purine foods (red meat, seafood, organ meat, shellfish, oily fish), beer, sugary beverages, obesity, metabolic syndrome, renal dysfunction, diuretics, baby ASA
Manifestations of gout
MSU crystals activate NLRP3 inflammasome in macrophages, release of IL-1β which leads to recruitment of neutrophils and other immune cells and amplifies the inflammatory response
Lab values associated with gout
-Uric Acid > 6.8
-Synovial Fluid Analysis
-Presence of negatively birefringent MSU crystals under polarized light
-↑ inflammatory markers (ESR, CRP)
Normal or ↑ WBC in acute attacks
Causes of OA
Mechanical stress/aging, breakdown of cartilage in joints which cause bones to rub against each other causing inflammation/pain
Risk factors of OA
Age, genetics (cartilage structure, bone density/quality), obesity, joint injury/overuse, poor posture
What joints are commonly affected in OA?
Large (knees/hips); middle / distal joints (DIP)
Causes of RA
Chronic autoimmune disorder that has persistent joint inflammation
Risk factors of RA
Genetics, environmental (smoking/infections), hormonal (post-menopausal), obesity, poor diet
Labs for RA
+ Rheumatoid Factor (RF)
+ Anti-CCPs antibodies
↑ ESR and CRP
Which joints are affected by RA?
Symmetrical, commonly affects small joints (wrists, MCPs, PIPs)
Pain occurs in the morning and improves with movement
Cause of Cushing’s
Excess cortisol
Long-term glucocorticoid use, small cell lung cancer, adrenal carcinoma
Common characteristics of Cushing’s
Weight gain, moon face, purple striae, muscle weakness
Complications of Cushing’s
HTN, hypokalemia, ↑ risk of heart disease, stroke, insulin resistance, obesity, dyslipidemia
Electrolyte imbalances of Cushing’s
Hypokalemia, hypernatremia, hypocalcemia
Primary Cushing’s
Excess cortisol is from issues with adrenals themselves
Secondary Cushing’s
Caused by ACTH-secreting tumors in the pituitary (typically BENIGN PITUITARY ADENOMA)
Causes of Addison’s
Adrenal glands do not produce enough hormones
Damage to adrenals from autoimmune disorders, infections, hemorrhages, and/or tumors
Common characteristics of Addison’s
BRONZE SKIN, weight loss, postural hypotension, decreased axillary/pubic hair, myalgia/arthralgia, depression, psychosis
Electrolyte Imbalances associated with Addison’s
Hyponatremia, hyperkalemia
What is primary hyperthyroidism?
Problem with gland itself producing hormone
What is secondary hyperthyroidism?
Problems with pituitary & hypothalamus
Negative feedback system of thyroid production
Hypothalamus releases TRH -> pituitary releases TSH -> thyroid produces T3 & T4
What is graves?
A type of hyperthyroidism, is autoimmune activation of thyroid-stimulating hormone receptor (TSHR) and antibodies mimic TSH which leads to overproduction of T3 & T4
Signs / Symptoms of Graves
↑ metabolism, weight loss, heat intolerance, tremors, palpitations, tachycardia, a fib
Ophthalmopathy, exopthalmos , periorbital edema, diplopia
Thyroid function tests of Graves
↓ TSH, ↑ T3 & T4; + TSI (thyroid stimulating immunoglobulin)
Risk factors of Graves
women, 30-50 years old, environmental triggers, stress, smoking, infections
Signs and symptoms of hypothyroidism
Tired, slow-growing / thin hair, myxedema coma (in severe cases)
What is Hashimotos
Autoimmune hypothyroid disorder, chronic lymphocytic infiltration of thyroid gland.
Signs / Symptoms of Hashimotos
Fatigue, weight gain, cold intolerance, constipation, pale/dry skin, depression, goiter,
Thyroid Function Tests in Hashimotos
↑ TSH, ↓ T4; + anti-TPO and anti-Tg antibodies
Which hormones are secreted by anterior pituitary?
FSH, LH, ACTH, TSH, GH, prolactin, and endorphins
Which hormones are secreted by posterior pituitary?
ADH and oxytocin
Complications of excess GH in childhood
Gigantism (large body parts, coarse facial features)
Complications of excess GH in adulthood
Acromegaly (enlarged bones and soft tissue, facial changes - brow, lower jaw)
Complications of low GH in childhood
Slow growth (< 2” / year) and short stature, immature features, chubby build
Complications of low GH in adulthood
“Dwarfism”
Defined as ≤ 4’10”
Hormones involved in stress response
CRH, ACTH, cortisol
Stages of Stress
- Alarm (ACUTE): activation of HPA axis, body releases adrenaline (epinephrine) and cortisol
- Resistance (CHRONIC): prolonged stress, body sustains energy levels, maintains heightened alertness, has gradual depletion of resources
- Exhaustion: body can no longer sustain stress, depletion of energy reserves; has impaired immune function and increased risk of chronic disease
Acute Stress
Short-term response (minutes-hours) to immediate danger or challenge
Secretes adrenaline and cortisol
Chronic Stress
Prolonged exposure (weeks-months) to stressors
Cortisol is released
What are osteocytes?
Mature osteoblasts
