Final exam Flashcards
mass effect
non-function and exert local pressure on gland or surrounding tissue, which can interrupt or alter function or slowly crush the tissue out of existence
effect of a growing mass that results in secondary pathological effects by pushing on or displacing surrounding tissue.
negative feedback loop
secreting hormones stimulate a target organ, which in turn secrets its own hormones to achieve the desired end effect
negative feedback loop organs (pituitary gland)
adrenal glands, thyroid, ovary, testies, release their own hormones for a final effect, these hormones in turn interact with the pituitary gland in a negative feedback loop
adrenal cortex
located on the tops of the kidneys, the outer cortex of the adrenal gland
secretes corticosteroids:
◦ mineralocorticoids- primarily aldosterone; secreted by the zona glomerulosa, they act on the kidney to retain sodium and water and excrete k+, actions that increase blood volume and regulate blood pressure
◦ glucocorticoids, mainly cortisol; secreted by the zona fasciculata
‣ increase glucose production
‣ stimulate the degradation of protein into amino acids and fat into fatty acids
‣ inhibit peripheral glucose utilization to ensure that adequate glucose is available for the brain
‣ suppress immune reaction and limit inflammation
◦ sex steroids
‣ estrogens and androgens, less potent than those secreted by the ovaries and testes
adrenal medulla
directly connected by nerve fibers of the autonomic nervous system
secretes hormones that act on cardiac muscle, smooth muscle, and glands to control involuntary functions such as heart rate, blood pressure, sweating, and bowel peristalsis
• formed of chromaffin cells: neuroendocrine cells derived from embryologic neural crest that develops into brain and peripheral nerves
• chemoreceptors sensitive to pH and oxygen tension in the regulation of respiration
• chromaffin cells secrete catecholamines, chemicals that act in various ways to help the body adapt to sudden stress
• epinephrine
◦ simulates heart rate
◦ dilated bronchioles
◦ coronary arteries
◦ constricts peripheral blood vessels
◦ increases mental alertness and respiratory rate
◦ increases metabolic rate
• norepinephrine
◦ powerful effect causes constriction of small blood vessels, increasing peripheral resistance and raising blood pressure
tumors can cause overproduction of catecholamines
parathyroid
not under control of pituitary gland
rather their output of parathyroid hormone (PTH) is controlled by the level of free ionized blood calcium
Regulates calcium homeostasis in a negative feedback loop with free calcium
• tumors-> usually lead to hypercalcemia due to increased PTH
DI
Diabetes insipidus
Hypofunction of the posterior pituitary: vasopressin deficit
excessive production of dilute urine
‣ high Na+
‣ high blood serum osmolality
head trauma, inflammatory disorders of the brain or pituitary, tumors, or pituitary surgery
‣ can also be nephrogenic DI
‣ low urine specific gravity
30% idiopathic 25% brain tumors 20% surgical tx of brain tumors 16% brain trauma 9% hypophysectomy
TX: desmopressin (DDVAP) monitor urine specific gravity, adequate fluid intake
SIADH
Hyperfunction of posterior pituitary: vasopressin excess
syndrome of inappropriate ADH secretion
‣ associated with excessive ADH production, usually from nonpituitary neoplasm
‣ brain, pulmonary and endocrine disorders
‣ hyponatermia and cerebral edema
tx: eliminate cause, correct volume blood abnormalities
euthyroid sick syndrome
patients with severe nonthyroidal illness may have abnormally low thyroid function tests but are clinically euthyroid
SICK, hospitalized patient that develops low thyroid test
Thyrotoxicosis
A hyper metabolic state caused by excess thyroid hormone- increased levels of T3 + T4 (no matter the source)
• lid lag
• heat intolerance
• overactive metabolism
• tachycardia
‣ diffuse glandular hyperplasia
• usually graves disease
‣ multi-nodular goiter with overproduction of hormones
‣ adenoma of the thyroid with overproduction of hormones t3
‣ speeds up cells metabolic rate
‣ increases cardiac output
‣ activates sympathetic nervous system
diagnosis
‣ measuring TSH, T3, T4
• primary cause->TSH will be low and unbound thyroid hormones will be high
‣ radioactive iodine uptake test
thyroid storm
state of severe hypermetabolism
graves disease
autoimmune disease caused by the production of multiple antithyroid antibodies
IgG autoantibodies (TSI) bind to and stimulate TSH recepors on thyroid
◦ most often affects women
◦ can be accompanied by other autoimmune diseases
◦ clinical findings
‣ hyperthyroid goiter due to diffuse thyroid hyperplasia
‣ pretibial infiltrative dermopathy
‣ ophthalmopathy
• exophthalmos (globe pushed forward)
- lab findings: increased T4/T3 levels and low TSH (make less!)
hypothyroidism
Underproduction of thyroid hormones by the thyroid gland
more common than hyperthyroidism
women more often affected
◦ primary- disorders within the gland
◦ secondary- disorders affecting pituitary or hypothalamus
◦ primary hypothyroidism-> due to thyroid gland problems (more common!) congenital, acquired, or autoimmune
- iodine deficiency
- hashimoto thyroiditis- autoimmune disorder
cretinism
hypothyroidism in children
congenital often caused by iodine deficiency in pregnancy
or genetic defects
myxedema
hypothyroidism that develops in the older child or adult
‣ thick myxomatous fluid in various organs
‣ bags under eyes, puffy eyelids, swollen tongue, edema of vocal cords and hoarseness, swelling of the hands and feet, pleural and pericardial effusions, weight gain, skin is cool and pale
‣ cold intolerance
Hashimoto thyroiditis
‣ chronic autoimmune disease, is by far the most common type of thyroiditis, hypothyroidism and goiter int he united states
‣ nontoxic goiter and almost elusively in mid aged women
‣ antithyroid antibodies and cytotoxic t cells destroy thyroid epithelial cells
‣ causes mild hypothyroidism
‣ patients are at risk to develop nonhodgkins lymphoma
tx: lifetime hormone replacement therapy with L-thyroxine
subacute granulomatous thyroiditis
‣ less common then Hashimoto
‣ may be associated with viral infections (URIs)
‣ much of reserve is released through inflammatory process, patients may become thyrotoxic for a short period of time as thyroid hormones are washed out of inflamed gland
goiter
is an enlarge thyroid gland. describes only the size of the gland and does not indicate anything about thyroid function or pathology
Cushing syndrome
adrenalcortical hyperfunction: clinical s/s that result from excessive amt of blood glucocorticoid, usually cortisol
exogenous (from glucocorticoid therapy) or endogenous
‣ the most common cause is exogenous glucocorticoid medical therapy
• medications mimic action of cortisol on tissue
• negative feedback, which shuts down
Primary: adrenal tumor Secondary: Pituitary adenomas=Cushing
disease( Ectopic ACTH production)
Tertiary – Hypothalamus malfunction
• Exogenous corticosteroid use
ACTH= usually produced by pituitary gland and controls the production of cortisol
s/s: htn, obesity, round (moon) facial features, DM, skin marks striae, excess body and facial hair (hirsutism), muscle wasting, bone demineralization, mensural and mental abnormalities.
adrenocortical hyperfunction, aldosterone effects, and androgen effects
labs: cortisol levels; plasma and urinary
tx: surgery (unilateral adrenalectomy), cortisol-blocking medications, weaning exogenous steroids as able
congenital adrenal hyperplasia
‣ congenital disorder of sexual differentiation that arises from one of the sever varieties of autosomal ressevice genetic defects that cause cortical enzyme deficiency, androgen excess, congenital adrenal hyperplasia
‣ 21 b-hydroxylase deficiency
‣ aldosterone deficiency and salt wasting
Addison disease
primary cortical failure-> deficiency in all 3 corticosteroids (cortisol, aldosterone, and sex steroids)
Primary:
◦Destruction of gland:
idiopathic, autoimmune, trauma, neoplasia
almost all cases attributed to: autoimmune adrenalitis, TB, AIDs, or metastatic carcinoma
Inability to adjust to
stress
◦Hypoglycemia
◦Weight loss
Insufficient
aldosterone
◦Low blood pressure
◦Weakness
◦Hyperkalemia
◦Hyponatremia
Increased ACTH
◦Hyperpigmentation
• tx- corticosteroid replacement/ lifetime cortisol replacement
addisons disease is rare
pheochromocytomas
‣ rare neoplasm of the adrenal medulla
‣ severe HTN- most important clinical sign
‣ benign tumors are surgically removed
produce catecholamines
s/s headache, tachycardia, diaphoresis
dx: ct scan- to see tumor?
tx: surgical removal of tumor
also..
◦ paragangliomas
‣ other neurogenic tumors that arise from chromaffin cells in the medulla or paraganglion system
hyperparathryroid
oversecretion of PTH by the parathyroid glands
‣ primary- parathyroid hyperplasia or adenoma
‣ secondary and teriary overactivity are due to chronic renal failure
‣ classical findings stones, bones, groans with psychiatric overtones
• kidney stones
• destructive bone changes and osteoporosis
• groans is peptic ulcers, pancreatitis, or gallstones that occur in some cases
• psychiatric overtones
◦ depression and fatigue
hypoparathyroid
low blood calcium and PTH levels
internal respiration
oxygen utilization / use of O2 b cells to release energy
Lung compliance
relationship between lung volume/ expandability and pressure / ease of inflation
compliance=change in volume/change in pressure
Forced vital capacity (FVC)
◦ volume measurement of air expelled from maximum inspiration to maximum expiration regardless of time it takes
◦ take deepest breath in and deepest breath out
◦ index of pulmonary function
Forced expiratory volume (FEV1)
◦ rate measurement
◦ the amt of air expelled from maximum inspiration in the first second of effort
FEV1/FVC ratio
◦ critical in separating obstructive and restrictive lung disease
◦ low=obstructive disease-> decreased FEV1 r/t to rate of air flowing out of lungs slowed , but lung volumes are usually normal or expanded
◦ ~normal= restrictive disease-> decreased FVC… both ratio of airflow to lung volume is near normal because restrictive disease limits both volume and flow rate proportionally
Spirometry
diagnostic procedure that measures lung volumes (capacity) and the flow rate (L per second) of air going into and out of the lung
enables clinical to differentiate between restrictive and obstructive disease
COPD
Chronic bronchitis and emphysema *
‣ emphysema
• irreversible destruction of alveolar walls and merging of alveoli to form large air spaces
• marked decrease of pulmonary membrane surface are and diffusion capacity
• unusually large air space is called a bleb or bulla
‣ chronic bronchitis
• chronic cough that produces sputum for three consecutive months two years in a row
• may lead to emphysema or right heart failure and is implicated as an added factor in the development of lung CA
◦ chronic air trapping caused by bronchial outflow obstruction
◦ most often caused by heavy smoking
Emphysema
pink puffers, emancipated smoker with dysnea
• Irreversible destruction of alveolar walls and
merging of alveoli to form large air spaces
• Decreased pulmonary membrane surface area and
diffusion capacity
• 90% of cases caused by smoking , 10% idiopathic
• Alpha-1 antitrypsin (protein that inhibits digestive
enzymes) is inhibited – lungs get destroyed
- gross anatomy of features of large air spaces especially in apex of each lung→ bulla or bleb
- lesion is in ALVEOLI
chronic bronchitis
• Clinical diagnosis
• Chronic productive cough for 3 consecutive months two years
in a row.
• Can lead to emphysema, right-sided failure, lung CA • Tobacco smoke, gases, fibers, grain dust can irritate bronchi
and stimulate chronic inflammation
• Area of attack is the bronchi and bronchioles
- Lesion is in bronchi and bronchioles
complications of COPD
Chronic hypoxia, pulmonary vasospasm, PH, cor pulmonale, right heart failure
Pulmonary HTN - hypoxic vasoconstriction
chronic bronchitis→ lung CA
emphasema- rupture of bulle → ptx
Sarcoidosis
• Systemic granulomatous disease (affects many tissues) • 10 x more frequent in AA than Caucasians • Unknown etiology
• Granulomas can appear anywhere – classically in lungs
and mediastinal lymph nodes • Skin lesions, lymphadenopathy, hepatosplenomegaly
• SOB, cough, chest pain, hemoptysis
• Can spontaneously recover • Prognosis poor for those with cardiac, brain, or
extensive lung involvement
- noncaseating granulomas (TB=caseating)
Pulmonary embolism
Pulmonary embolus is undissolved, detached material
◦Blood clot
◦Fat emboli
◦Amniotic fluid
◦Occludes blood vessels
Predisposed by Virchow’s triad:
◦Venous stasis
◦Hypercoagulability
◦Intimal injury
Pneumonia
- Inflammatory reaction in the alveoli and interstitium caused by an infectious agent
- causes: Aspiration or inhaled (chemical pneumonia) – anaerobic oral flora
• Infection (acute vs. chronic – TB, histoplasmosis) - most PNA is community acquired
agents of PNA
Community acquired vs. hospital acquired
• Bacterial
• Gram + Staphylococcus, streptococcus
• Gram – Haemophilus influenza, Klebsiella, Pseudomonas aeruginosa,
Serratia marcescens, Esherichia coli and Proteus species
• Viral
• Legionella or Mycoplasma • Fungal
• Pneumocystis carinii and other opportunistic pathogens
lung neoplasms
Bronchogenic carcinoma is the most common
fatal malignancy in the world.
◦Small cell carcinoma
◦Non-small cell carcinoma
◦Adenocarcinoma
◦Squamous cell carcinoma
◦Large cell carcinoma
2 anatomic forms of PNA
- bronchopneumonia
characterized b patchy, noncontiguous inflammation, usually involves the alveoli of more than one lobe
- lobar pneumonia
characterized by intense, consolidated acute inflammation of the alveoli in an entire lobes and is the form that is much more likely to occur in patients with CHF, COPD, DM, alcoholism
The most common agent in community acquired PNA
s. pneumoniae
primary atypical pneumonia (PAP)
- cause interstitial rather than alveolar inflammation
- in most cases the agent cannot be proven
- when the agent is identified, it is usually mycoplasma, chlamydia, rickettsia
chronic PNA
is usually due to tuberculosis or deep mycosis.
usually localized to a single lobe
Small cell carcinoma
- most lethal and resistent to therapy
- derived from neuroendocrine cells of the bronchial mucosa
- occurs almost exclusively in smokers
- composed of distinctive small, dark, cells that look much like large lymphocytes
- aggressively malignant
non-small cell carcinomas
- adenocarcinoma
- squamous cell carcinoma
- large cell carcinoma
adenocarcinoma
formed into glandular acini
the most well-differentiated lung Cas, slightly better prognosis than other non-small cell CA
- tend to occur in the small bronchi
squamous cell carcinoma
composed of malignant cells that differentiate toward flat (squamous) cells like the epithelium of the epidermis, mouth, and esophagus..
- tend to arise centrally in the main bronchi near critical mediastinal structure and therefore may not be as easy to remove surgically as other types
large cell carcinomas
composed of large, fleshy, rounded or elongated cells that lack differentiation toward any particular type of tissue and probably represent squamous carcinomas or adenocarcinomas that are too undifferentiated to permit specific classification
paraneoplastic syndromes of lung CA
systemic symptoms owing to tumor secretion of hormones or other substances
- small cell carcinoma is particularly likely to produce paraneoplastic syndrome
- hypercalcemia, migratory thrombophlebitis, hypercortisolism (cushings), and neurologic syndromes such as encephalopathy
ARDS
- injury to vascular endothelium and alveoli
- acute inflammatory fxn ensues
- pneumocytes die and microthrombi form in capilaries
- neutrophils infiltrate the alveolar wall and protein rich fluid exudes into alveolar space
- stiffins the lung, and limits airflow, which interfers with gas diffusion
- fatality rate ~ 40%
- secondary pna is a common complication, protein rich exudate invites microorganisms
- after initial phase->fibrous repair begins in the interstitium,
- this may proceed to interstitial fibrosis
asthma
chronic inflammatory disease/ obstructive disorder
of bronchioles that is characterized by recurring episodes of bronchospasm and excessive production of mucus
◦ atopic (allergic), irritant stimulates type I hypersensitivity
◦ nonatopic
‣ other factors may precipitate attack suck as uri, strenuous exercise, drug reaction, severe air pollution
‣ occupational asthma
◦ recurrent episodes induce permanent remodling of the airway, characterized by hyperplastic mucus glands, mucus plugs, and hypertrophied bronchial smooth muscles, edema, and marked eosinophilic inflammation
◦ status asthmaticus, severe prolonged state of asthmatic bronchospasm, life threatening
interstitial pneumonia
inflammation confined to the alveolar septa, usually caused by virus
infectious rhinitis
“common cold”
◦ symptoms usually disappear in about one week
◦ uncomplicated URIs are viral
◦ appearance of yellow purulent nasal discharge or ear or sinus pain usually signifies secondary bacterial infection
almost always viral
mild fever, mucosal congestion, watery, clear nasal discharge
allergic rhinitis
Hay fever
◦ affects 20% of population
◦ exaggerated immune reaction
allergic conjunctivitis may also occur
nasal polyps
recurrent rhinitis of any type may lead to nasal polyps
can block normal drainage
exaggerated folds of edematous mucosa with inflammation and epithelial hyperplasia
tx is surgical excision
laryngitis
loss of voice, usually viral
laryngitis
loss of voice, usually viral
acute sinusitis
pain, nasal drainage, congestion, fullness, and fever
(tolerate for 10 days before prescribing antibiotics)
pharyngitis/ tonsillitis
◦ inflammations of the throat that are usually viral
◦ group A streptococcus, acute streptococcal pharyngitis can result in autoimmune reaction_> acute rheumatic fever or acute glomerulonephritis
vocal cord nodules
polyps benign, small smooth fibrous nodules caused by smoking or chronic vocal stress
(singers node)
carcinoma of the larynx
smoking and ETOH risk factors
lesion begins as hyperplasia of laryngeal squamous mucosa and develops through progressive stages of dysplasia, carcinoma in situ, and invasive carcinoma
parathyroid gland
regulate calcium metabolism
posterior pituitary secretes..
- ADH
- oxytocin
(synthesized in the hypothalamus then travels down the nerve axons within pituitary stalk to the posterior pituitary- where they are stored in the tips of axons, upon receiving hypothalamic nerve impulse, hormones are released directly into systemic circulation)
anterior pituitary cells
- somatotrophs→growth hormones
- lactotrophs→prolactin
- corticotrophs→pro-opiomelanocortin
- thyrorophs→TSH
- gonadotrophs→FSH/LH
negative feedback loops:
adrenal glands, thyroid gland, ovary, testis
growth hormone deficiency
Growth Hormone Deficiency 10,000-15,000 in US (1:3500 live births)
Normal birth size Hypoglycemia
Normal growth through 6 months
Proportional short stature Delayed puberty common
Fat around waist and in face
Higher pitched voice
Hypoglycemia
Younger appearance
Decreased muscle mass
Delayed
◦ Skeletal maturation
◦ Dentition
◦ Onset of puberty
“falling off the growth chart”
TX: growth hormone replacement
side effects:
◦Musculoskeletal pain
◦Reduced insulin sensitivity
◦Gynecomastia
◦Hypothyroidism
◦Pancreatitis
◦Adrenal insufficiency
Acromegaly
Excessive GH production
◦Enlarged hands and feet
◦Growth of facial bones
◦Organ enlargement
◦Diabetes mellitus
growth in the hands, feets, face, skull, and jaw; growth of liver, heart, thyroid, adrenals, and other viscera
occurs in adult whom growth plates have fused
gigantism
general increase in body size, with especially long arms and legs, occurs when child or teenager develops an adenoma that secretes GH before growth plates close at the ends of long bones
Transsphenoidal Hypophysectomy
Transsphenoidal hypophysectomy is a commonly used surgical approach for pituitary region masses, with many significant advantages over open craniotomy.
growth hormone adenomas
secrete GH, and are second only to prolactinomas among functioning adenomas of the anterior pituitary
often diagnosised due to mass effect and may become quite large
thyroid negative feedback loop
labs in thyroid disease
*Hyperthyroid- TSH is low because T4 is high and you need to make less!
*hypothyroidism (primary) - TSH high because you need to make more! T4 is low which is a problem..
*hypothyroidism (secondary)-
TSH low, problem is higher up, which makes T4 low too
hyperthyroidism labs
- Elevated free T4
• With normal or high TSH:
secondary
• With low TSH: primary
• With anti-TSH IgG: Graves
disease
hyperthyroidism tx
- Anti-thyroid hormone medication
- Propylthiouracil (PTU)
- Methimazole
• Symptom control with beta blockers
Counter SNS symptoms
Inhibit T4 T3 conversion
• RAIU ablation→ May need thyroid replacement (when antithyroid drugs don’t work)
adrenal function
Cushing disease
when cushing s/s caused by ACTH secreting adenoma
named after Harvey cushing who pioneered describing the affects of ACTH secreting adenoma
hormonal and neural signals involved in digestion
causes of GI bleeding
Upper GI bleeding
lower GI bleeding
colorectal intestinal bleeding
hematochezia
red blood mixed with stool
melena
black stool, can be from any intestinal site including esophagus
occult
not visible to naked eye- great for detecting slow bleedings for colon CA screening
mallory-weiss tear
severe and frequent retching or vomiting may cause esophageal/ or gastric laceration
lacerations are usually near the gastroesophageal junction
achalasia
spasm of the lower esophageal sphincter
motility disorder
tx: dilation, chemical denervation of remaining autonomic connections, and surgery to release spastic muscle fibers
hiatal hernia
protrusion of part of stomach into the chest through the esophageal hiatus
esophagitis
inflammation of the esophagus
ETOH and smoking risk factors
chest pain and painful swallowing are common
tx, correction of underlying disorder and antimicrobial therapy if appropriate
GERD
due to chronic reflux of gastric acid into the lower esophagus (LES)
◦ 30% of US population is affected
◦ incompetent lower esophageal sphincter
◦ anatomic abnormality, esophageal hiatus, obesity, etoh, smoking, caffeine, high fat diet, certain drugs known to relax the LES
◦ heartburn common symptom
complication~ Barrett metaplasia/ barrett esophagus
‣ change (metaplasia) of esophageal epithelium from squamous to columnar
tx:
◦Histamine (H2)-blocker - occasional
◦Proton pump inhibitor (PPI) – chronic
◦Can halt or reverse changes
◦Endoscopic dilatation of strictures
◦Nissen fundoplication - intractable
Barretts esophagus
Cellular changes that increase the risk for esophageal cancer
• metaplastic changes: Normal squamous epithelium becomes replaced with types of columnar cells
- Risk factors:
- Chronic heartburn and acid reflux
- Age
- Being a man
- Being white
- Being overweight
- Current or past smoking history.
precursor condition associated with increased risk of esophageal adenocarcinoma
pyloric stenosis
obstruction of the stomach outlet due to hypertrophy of the sphincter muscle
affects1 in 250 newborns
bile-free-projectile vomiting shortly after eating
acute gastritis
Inflammation of stomach lining
• H. Pylori, ETOH, stress, chronic NSAID use, autoimmune
• Types:
• Non-erosive – transient inflammation (no ulceration!)
NSAIDs, ETOH, steroids, chemo, age-related changes
• Erosive – more severe! Trauma, sepsis, burns, etc. (upper abd. Pain, nausea, vomiting, sometimes bleeding)
chronic gastritis
Infection, or autoimmune
• Often asymptomatic
• H. Pylori, smoking, ETOH, autoimmune gastritis (pernicious
anemia)
- H. Pylori = must eradicate with multi-drug therapy!
- Proof of cure is with the breath test.
Peptic ulcer disease
◦ Caused by action of acid and pepsin
◦ Injury to the mucosa of the esophagus, stomach, or
duodenum
◦ Range from a slight mucosal to severe ulceration
◦ Increase in factors that tend to injure the mucosa
relative to factors that tend to protect it
Causes
◦ No relation between diet and PUD
◦ NSAIDs, stress, steroids (glucocorticoids), smoking,
genetics
◦ H. pylori
◦ Key role in ulcer formation
◦ Thrives in acidic conditions
◦ Clearance of H. pylori promotes ulcer healing
dx:
◦Upper GI barium contrast radiography or by endoscopy
◦Endoscopy
◦Testing for H. pylori
Treatment
Reducing gastric acidity
Prevent recurrence
H. pylori antibiotics
H2 antagonists
Proton pump inhibitors
Sucralfate (forms protective coating over injured mucosa)
Ulcerative colitis
- colon only
- rectal bleeding common
- no fistulas
- no skipped areas
- inflammation in muscosa
- no granulomas
Pathophysiology Inflammation begins > at base of crypts of Lieberkühn
◦Formation of abscesses in crypts
◦Abscesses coalesce
◦Large ulcerations develop in epithelium
Continuous - linear
crohns disease
- anywhere in the GI tract
- rectal bleeding uncommon
- fistulas common
- skipped areas
- full thickness inflammation
- granulomas common
inflammatory bowel disease
- bloody diarrhea
- lower abdominal pain- colicky
- fulminant colitis and toxic megacolon (10 stools per day, distension, fever)
- arthritis
inflammatory bowel disease
chronic inflammation at various sites in the GI tract
crohns disease and UC are closely related conditions cause by immune-mediated inflammation
- Crohns disease
- ulcerative colitis
irritable bowel syndrome
combination of intestinal syndromes that are difficult to define
alternating constipation and diarrhea/ abd cramping pain
offers no objective pathological findings or laboratory abnormalities
necrotizing enterocolitis
inflammation in the bowel of a preterm or low birthweight infant
characterized by diffuse or patchy intestinal necrosis and sepsis
bowel ischemia
illeus
Peristalsis is interrupted
- Post-op
- Appendicitis, gallbladder disease
- Intestinal ischemia
- Post spinal cord injury
• Hypokalemia
• Signs/Sx:
• Vomiting, abdominal pain, lack of BMs,
hypoactive bowel sounds
• Characteristic horizontal air-filled interfaces on
xray.
causes of mechanical obstruction
- adhesions
- intussusception
- volvulus
- herniation
increased bowel sounds
initially (then hypoactive or absent), accompanied by
abdominal pain, nausea, and vomiting
congenital megacolon/ Hirschsprung disease
1 in 5,000 live births
no peristalsis occurs in affected segment, feces cannot pass, upstream colon distends with fecal matter
gastroschisis
congenital abnormality
intestines and other viscera protrude through the largely absent abdominal wall
r/t to omphalocele, but a larger defect
omphalocele
midline defect in which herniated viscera are covered by a thin peritoneal membrane
may be small or may contain most of abdominal viscera
1 in 2,000 live births
hemorrhoids
- Constipation
- Venous stasis in pregnancy
- Painful
- Itchy
- Bleeding (bright red)
• OTC ointments, warm baths, surgical
excision.
Complications:
• Thrombosis, strangulation, and
infarct
staging of colorectal CA
adenomatous polyps
- Premalignant
- Half in rectosigmoid colon
- 10-15 years can become fully malignant and spread
• Asymptomatic at first, then bleed (fecal occult
blood test!)
diverticulosis
characterized by small, multiple, outward protrusions of colonic mucosa through the muscular wall that arise at the weak points where small blood vessels penetrate from the external surface
“outpouchings”
diverticulitis
inflamed diverticulum. Trap feces or seeds which irritate, inflame, and allow bacteria to invade.
Fever, left-side abdominal pain.
• Perforation can cause peritonitis.
• Abdominal imaging is conclusive.
• Tx: liquid diet, broad-spectrum antibiotics, increase fiber.
digestion
mechanical digestion: teeth slicing, tear, or crushing food
(~ broken down by→to)
proteins/peptides~proteases→amino acids
carbohydrates~amylases, saccharidases, others→monosaccharides
lipid/triglyceride~lipases→ glycerol and fatty acids→clustered by epithelial cells into lipoproteins called chylomicrons→ transported to the liver, muscle, or fatty tissues where they are metabolized
cholesterol is a sterol, closely related to steroid molecules like testosterone and estrogen, absorbed directly by intestinal epithelium
Functions of the liver
- Carbohydrates: glucose << >> glycogen
- Lipid: synthesize lipoprotein; TG >> FFA + glucose + cholesterol
- Protein: synthesize albumin, coagulation factors, others
- Waste disposal: bilirubin, cholesterol >> bile acids, ammonia, drugs, toxins
- Storage: glycogen, fat, vitamins, iron
endocrine & exocrine functions
Liver function tests
- AST & ALT- released with hepatocyte injury/ marker of hepatic inflammation (like cardiac enzymes)
- albumin, indicative of chronic liver injury (20 day half-life)
- bilirubin- if hemolytic disease is excluded, increased levels of blood bilirubin usually indicates at least moderate liver or bile duct disease
- PT/ coagulation tests- liver disease can cause prolonged abnormal PT and PTT times
jaundice
conjugated bilirubin is water soluble (readly excreted into bile/urine)
unconjugated is not water soluble (not readly excreted in bile)
Liver waste disposal
unconjugated is not water soluble (not readily excreted in bile) tightly bound to albumin for trasnport to lever
conjugated bilirubin is water soluble (readily excreted into bile/urine) jointed to glucuronide
liver clears blood of ammonia (a biproduct of protein metabolism)→ converting it into urea to be excreted by kidneys
cholesterol into bile acids→ main constituent of bile (most bile acids/ cholesterol are reabsorbed by the intestinal mucosa and returned to the blood- enterohepatic circulation)
cholestasis
obstruction of bile excretion
“jaundice is usually accompanied by cholestasis” also, pruritus because of deposition of bile acids in the skin; xanthomas from cholesterol deposits in skin
can be caused by intrahepatic or extrahepatic bile flow obstruction or by defective hepatocyte bile secretion
may result from: liver disease, biliary obstruction, drug interference with bile secretion, pregnancy, and a variety of other conditions
hepatic portal vein
The portal veinous system gains its name from the liver acting as a gate (a portal) through which blood must pass before entering the general circulation
hepatic portal vein: moves blood from the spleen and intestines to the liver for filtration and processing 75% of blood supply going into liver
kupffer cells
venous sinusoid walls contain fixed macrophages which unlike other macrophages, do not move but remain fixed in place to filter portal blood
portal triads
- a branch of the hepatic artery brining blood from the aorta
- a portal vein carrying blood from the GI tract
- small vile duct that carries bile out of liver
cirrhosis
- widespread scarring of the liver
- progressive, irreversible, incurable (end stage of many chronic liver diseases)
- associated with portal HTN (hepatic obstruction)
- 65% ETOH/chronic viral hepatitis
- 25% unknown etiology
- increasing=cirrhosis caused by fatty liver disease from obesity
- 3 dimensional web of interconnecting bands of scar tissue that divide the liver into small nodules of viable liver lobules, the trapped lobules attempt to regenerate, and they well to form nodules
2 types of cirrhosis
- portal cirrhosis: the most common, caused by chronic diffuse li ver cell injury, such as ETOH/or hepatitis, scar tissue disrupts the lobular anatomy and does not follow to anatomic outlines of the lobules
- biliary cirrhosis: uncommon and is caused by chronic disease of the biliary tree, such as primary biliary cirrhosis or chronic biliary obstruction and inflammation
fatty liver
fatty degeneration of hepatocytes also known as steatosis
liver is enlarged, x2-3, yellow, greasy
reversible, but scarring/cirrhosis is not
portal HTN
increased BP in portal venous system (pre, post, hepatic)
consequences: ascites, splenomegaly, portosystemic shunts/ varices (lower esophagus, stomach, rectum), caput medusa, hepatic encephalopathy, asterixis (hepatic flap)
hepatic failure
loss of hepatic metabolic function severe enough to cause hepatic encephalopathy
destruction of 80-90% of function capacity is required
without transplant, over 80% of cases are fatal
s/s: bilirubin excretion fails and jaundice appears, low blood albumin encoureges acites (which can become infected>BP), musty and breath odor, fecor hepaticus, spider angiomas, gynocomastia/ hypogonadism, coagulation defects, hepatic encephalopathy, asterixis
hepatorenal syndrome
development of renal failure in a patient
Hepatitis A
epidemic hepatitis, most common hepatitis worldwide. self limited disease
transmission: fecal-oral
incubation: 3-6 weeks
carrier state: no
chronic hepatitis: no
fulminant hepatitis(severe liver impairment): no
Hepatitis B
infected ⅓ of world population
most are asymptomatic, or mild consitutional sx without jaundice
symptomatic infection = acute hepatitis and resolves with supportive care
transmission: parenteral, close contact
incubation: 2 weeks- 6 mo
carrier state: yes <1%
chronic hepatitis: 5-10%
fulminant hepatitis: yes
hepatocellular carcinoma:
hepatitis C
HCV= major cause of liver disease
most common blood borne infection in the US
transmission: parenteral or close contact
incubation: 2 weeks-6 months
carrier state: yes 10-40%
chronic hepatitis: >50%
fulminant hepatitis: rare
hepatocellular carcinoma: yes
c= chronic/ or cancer
tx: combo of anti-viral drugs, cure rates 70-80% are possible
nonviral inflammatory liver disease
abscess: bacterial- fever/hepatomegaly, mortality high
amoebic, unwashed food, craw up portal vein
autoimmune hepatitis: chronic, progressive. 20% chronic hepatitis, delayed t cell mediated, tx= immunosuppressive
liver injury
- jaundice and cholestasis
- cirrhosis
- portal HTN
- hepatic failure
toxic liver injury
dose-related: Tylenol
non dose related= “tipping point” for particular person (idiosyncratic)
reyes syndrome: related to ASA, combination of a fatty liver and acute brain dysfunction in children that develops after a viral illness treated with ASA. severe vomiting, lethargy, irritability, hepatomegaly, 25% progress to coma
alcoholic hepatitis
more severe form of liver injury than fatty liver
patholic finding=steatohepatitis (steatosis inflammation, hepatocyte necrosis, early fibrosis)
nonalcoholic steatohepatitis (NASH)
may progress to cirrhosis and is probably the cause of most unknown origin cirrhosis
wilson disease
rare autosomal recessive inherited disorder that results in impaired excretion of copper into bile, failure of copper to attack to ceruloplasmin, and failure of ceruloplasmin secretion into the blood
toxic accumulation of copper
kayser-fleischer ring- acute or chronic liver disease, behavioral oddities, psychosis, tremors, abnormal gait
hepatocellular carcinoma
HBV, HCV infections
elevated AFP
poor prognosis, cachexia, hepatic coma, GI bleeding
cholangiocarcinoma
malignancy of bile duct (common in asia/ SE asia)
agressive
cachexia, hepatic coma, esophageal varices, only 15% survive to 2 years
cholelithiasis
collectively, stones in the gallbladder or biliary tree
choledocholithiasis
stones in the bile ducts
cholecystitis
inflammation of the galbladder
acute cholecystitis with empyema
• Inflammation of the gallbladder
• >90% are associated with stone obstruction at
gallbladder neck
• Bacterial infection will eventually develop
• RUQ Pain, colicky pain, fever, nausea, vomiting,
leukocytosis, jaundice.
• Most attacks resolve, but about 25% require
emergent surgery.
Chronic cholecystitis and cholelithiasis
• Develops after numerous acute attacks.
• RUQ pain, nausea, vomiting • Intolerance for fatty foods (stimulates the
gallbladder to contract)
• Surgery (prevent septicemia, perforation)
Murphy’s sign
pain on inspiration RUQ- indicative of gal bladder issue
cholesterol gallstones
the most common
semitranslucent, yellowish, egg shaped
arise only in the gallbladder
pigmented gallstones
account for the remaining gallstones
20% of gallstones
composed of bilirubin, and bile substances other than cholesterol
risk factors: hemolytic anemia/ sickle cell anemia
pancreatic exocrine/endocrine fxns
exocrine
- Protease secreted as inactive enzyme (zymogen)
- Lipase and amylase secreted as active enzyme
endocrine
• Alpha cells: glucagon. Functional opposite of insulin,
stimulates liver glycogen >> glucose. Raises blood glucose • Beta cells: insulin & amylin. Opens cell membrane to glucose. Lowers
blood glucose
• Delta cells: somatostatin. Inhibits glycogen formation and
insulin secretion. Raises blood glucose
• PP cells: pancreatic polypeptide, acts on stomach to
stimulate juices and slow intestinal motility
glucagon
secreted by alpha cells
if blood glucose is low, glucagon will:
- stimulate liver to convert stored glycogen to useful glucose
- stimulate production of glucose from amino acids
- stimulate breakdown of fat into ketones
glucagon / glycogen / insulin metabolism
acute pancreatitis
acute, reversible, inflammation of the pancreas
risk: ETOH, gallstones, idiopathic, other causes including viral/ blunt truama/ thiazide diruetics, high blood levels of lipids
most severe form- acute hemorrhagic pancreatitis
s/s: • severe upper abdominal pain (radiates through back)
• Anorexia, nausea, vomiting
• Can decompensate quickly (vascular collapse, and DIC)
• Renal failure and ARDs can develop
• Bloody necrotic tissue can become infected
amylase / lipase
amylase- rise and fall quickly. found in high concentration in pancreas in salivary glands, and even minor inflammation or injury to either one causes release of significant amts of amylase into the bloodstream. highly sensitive, but not as specific
lipase- slow to rise but stay high for days to weeks after amylase returns to normal. more specific
chronic pancreatitis
repeated episodes of symptomatic or subclinical acute pancreatitis that cause irreversible destruction and scarring
chronic etoh abuse is a major contributing factor in ⅔ cases, l also play role
s/s: • obscure, nagging upper quadrant pain radiating through to
the back
- Mild fever and elevation of blood amylase (can occur)
- May get mild jaundice
- Weight loss
- May develop diabetes (destruction of islets of Langerhans
Diagnosis:
◦in children (often a manifestation of cystic fibrosis)
◦Elevated amylase and lipase (but can also be normal d/t so much destruction within the
gland!)
◦Abdominal ultrasound
Treatment:
◦fasting, alcohol abstinence, IV fluids and nutrition, analgesia, oral pancreatic enzyme
supplementation, surgical drainage or relief of obstruction. ◦Within 5 years, 50% of patients will die.
complications of DM
cardiovascular, renal, neural, and ophthalmic
mainly caused by hyperglycemia
glycoproteins>>accelerate atherosclerosis, cause DM microangiopathy, retinal and kidney disease
- atherosclerosis
- MI
- CVA
- gangrene
- diabetic retinopathy
- diabetic nephropathy
- diabetic neuropathy
DM dx
- classic symptoms- polyuria, polydipsia, polyphagia; unexplained weight loss- plus random blood glucose >200 OR
- fasting >blood glucose >126 OR
- blood glucose >200 2 hrs after carb load
DM2
- decreased sensitivity of peripheral cells to the effect of insulin (insulin resistance)
- beta-cell dysfunction that prevents adequate insulin response to decreased peripheral cell sensitivity and high blood glucose
- islets gradually replaced by amyloid, an abnormal protein
DM1
- Autoimmune disorder
- Destruction of islets of Langerhans and ABSOLUTE LACK OF INSULIN!
- About 10% cases
- Most diagnosed < 20 years old (“juvenile diabetes”)
- Genetic component
- More often in Northern European descent
- ? Viral illnesses (mumps, Coxsackie, rubella, CMV)
- Evaluate for DKA
- Kussmaul breathing
- Can have a diabetic coma, death
ketoacidosis
in absence of glucose, the body must burn fat for fuel
fat is broken down>> fatty acids>>transported to liver >> converted into ketones
unburned ketones excreted in urine and blown off by lungs
rapid, deep breathing; glycosuria; acidosis; ketonuria; osmotic diuresis; volume depletion; total body sodium and potassium depletion
ketoacidosis
in absence of glucose, the body must burn fat for fuel
fat is broken down>> fatty acids>>transported to liver >> converted into ketones
unburned ketones excreted in urine and blown off by lungs
rapid, deep breathing; glycosuria; acidosis; ketonuria; osmotic diuresis; volume depletion; total body sodium and potassium depletion
A1C
slowly metabolized and shows an index of average blood glucose over the last 120 days
pancreatic carcinoma
arise in the exocrine pancreas
½ of patients die within 3 months of dx, 5% survive to 5 years
smoking increases risk
usually causes few symptoms until its too late
5 functions of the kidney
- excretion of metabolic waste
- adjustment of blood pH by excretion of more or less acid
- adjustment of plasma salt concentration (plasma osmolality) by excretion of more or less salt and water
- adjustment of blood volume and blood pressure by secretion of renin
- stimulation of RBC production by secretion of erythropoietin
ADH
produced by hypothalamus in response to plasma osmolality and blood volume→ released by posterior pituitary
drives H20 reabsorption in the collecting ducts / distal convoluted tubule increases type 2 aquaporin channels
also binds to ADH receptors on blood vessels that causes vasoconstriction/ increased peripheral resistance
aldosterone
product of RASS system
works @ distal convoluted tubule
increases Na+/K+ atpase
increases Na+ reuptake→ water follows
decreases k+
BUN
blood urea nitrogen
synthesized in liver as product of protein metabolism
marker of hydration
the ratio of BUN/ Cr is usually between 10:1 and 20:1, an increased ratio may be due to a condition that causes a decrease in flow of blood to the kidneys such as CHF and dehydration
normal~6-24
juxtaglomerular apparatus (JGA)
the afferent arteriole and a small adjacent segment of the distal convoluted tubule combine to form the JGA
the JGA senses BP and blood flow in the afferent arteriole and sodium concentration in the distal convoluted tubule, and secretes RENIN as the first step in the RASS system
Cr
product of protein breakdown and also passes freely into the GF, but does not depend on liver metabolism; directly related to glomerular function and is more reliable indicator of renal performance
urine dipstick
Nitrates: produced by GN bacterial metabolism
casts= always indicate renal disease, cylindrical formations of compacted protein, red or white cells, or epithelial cells in the lumen of renal tubules
ketones: breakdown of fatty acids>> DKA
hemaglobinuria: + when no RBCs seen when spun, can be hemolytic anemia
proteinuria: transient is normal in 5% of people
Urolithiasis
/ nephrolithiasis
kidney stones
types: calcium, magnesium, uric acid, cystine
s/s: pain, bleeding, flank pain, cramping, renal colic
gold standard= CT scan
nephrolithiasis: stone in renal pelvis
hematuria
renal carcinoma until proven otherwise
tx: nephroctomy
cystitis
inflammation of the bladder
bacterial cystitis is the most common form of UTI
usually GN like E coli
complication~pylonephritis
nonbacterial cystitis
interstitial cystitis
bladder inflammation without infection
painful chronic cystitis involving all layers of the bladder wall
features intense chronic inflammation and mucosal ulcers (hunner ulcers)
can be caused by autoimmune / SLE
urethritis
inflammation of the urethra
STIs are common cause gonorrhea and chlamydia
urge incontinence
uncontrolled leakage of moderate to large urine volume after a quick developing and uncontrollable urge to void
most common type in the elderly
stress incontinence
urine leakage due to an abrupt increase of intraabdominal pressure- sneezing, coughing, lifting, laughing
overflow incontinence
dribbling from an overly full bladder
functional incontience
urine loss due to cognitive or physical impairment such as dementia or stroke
azotemia
renal failure that is manifested only by abnormal laboratory tests, no clinical signs of kidney failure is present
increased BUN & Cr
◦ Prerenal – decreased blood flow to the kidneys
(shock, dehydration, hemorrhage, etc.)
◦ Intrarenal – direct damage to the kidneys
◦ Postrenal – caused by obstruction of urine flow
from the kidney
uremia
“urine in blood” is renal failure that is manifested not only with increased nitrogenous wastes in the blood, but also with clinical s/s
HTN, anemia, edema, oliguria, pericarditis, gasteroenteritis, bleeding/coagulation defects caused by PLT malfxn, peripheral nerve disease
horseshoe kidney
single fused kidney
abnormal embryogensis
often seen in pts with turner syndrome
multi-cystic renal dysplasia
sporadic developmental disorder in which the fetal kidney develops as a small mass of cysts accompanied by islands of primitive cartilage and other immature tissue, usually unilateral
simple cyst
most are just a few mm in diamter, filled with fluid, larger ones can be incidentally found on radiographic exams and appear as a kidney mass
polycystic kidney disease
autosomal dominent polycystic kidney disease- often not symptomatic until adulthood (adult polycystic disease)
most need kidney transplant
fairly common, accounts for 10% of pts with kidney failure
autosomal recessive polycystic kidney disease is caused by one of several autosomal recessive genetic defects and usually appears at birth as massively enlarged kidneys a variety of other defects “childhood polycystic kidney disease” most infants die in parinatal period
nephritic syndrome
glomerular inflammation
usually acute
immune complexes
allows RBCs/ WBCs/ protein to come through
hematuria, proteinuria, RBCs casts in urine, HTN, edema, azotemia, oliguria (glomerulus damaged/low GFR)
>>poststreptococcal glomerulonephritis
nephrotic syndrome
marked proteinuria and severe generalized osmotic edema due to low plasma albumin secondary to protein loss
problem with basement membrane or podocytes to cause protein to leak out
marked proteinuria >3.5gm/day, marked hypoalbuminemia, marked generalized edema, hyperlipidemia, lipiduria
glomerulonephritis
almost all primary glomerular disease is autoimmune
type III & II hypersensitivity
male infertility
35% of couples=sperm disorders
impaired spermatogenesis: hypothyroidism or other endocrine disorders, infections of the testis or epididymis, undescended testies, variocele, drugs including estrogen, steroids, ilicit drugs
impaired sperm emission: dm neuropathy, prostatectomy, obstruction of vas deferens, genetic conditions, retrograde ejaculation
clomiphene (antiestrogen)
priapism
persistent painful erection
idiopathic causes
sickle cell anemia
anticoagulent therapy
phimosis
uncircumcised foreskin cannot be retracted
paraphimosis
retracted foreskin cannot be replaced
hydrocele
fluid collection around testicle or spermatic cord
acquired
scrotal injury
radiation therapy
infection of epididymis
transilluminates
tx: surgical drainage if painful
varicocele
scrotal varicose veins
scrotal enlargement and possibly infertility
tx: possible surgery
cryptorchidism
failure of the fetal tesis to descend into the scrotum
epididymitis
inflammation of the epididymis
in men under 35, cause is usually STI
in men older than 35, usually urinary pathogens
tx=antibiotics
dull achy pain in testicle
testicular torsion
twisting of spermatic cord (torsion)
infarction of the testies follows very painful
dx: clinical/US
tx: immediate surgical exploration and unwinding along with fixation (orchipexy of both testicles)
prostatitis
inflammation of the prostate
acute or chronic bacterial
E.coli most commonly
non-bacterial
routes of infection: reflux of urine, urinary catheter, instrumentation of the lower urinary tract
s/s: fever, chills, low back pain, acute prostatitis, frequency, urgency, dysuria
rectal exam- tender swollen prostate
abx= 4-6 weeks
cervicitis
acute: usually young women, infecious, STI-gonorrhea, chlamydia, herpes, or other STI
chronic- more common and usually asympatomatic
defer pap smear when someone comes in for symptoms until they don’t have symptoms since there will be changes
mastitis
• uncommon, most all cases are caused by infection in
lactating women.
• Typically = staph aureus or strep. Can produce an abscess.
• Diagnosis: can have fever, pain, malaise, vomiting,
lymphadenopathy. Diagnose clinically.
• Treatment = compresses, anti-inflammatories, frequent
breastfeeding/breast emptying, antibiotics
- Consider if breastfeeding
- Evaluate for abscess involvement
osteoblasts
bone forming cells create matrix of calcium salts and collagen fibers
form bone by depositing a network of bone matrix protein fibers called osteoid, unmineralized bond (osteoid)
osteoclasts
bone-dissolving cells, help with bone absorption, remodeling and repair, regulate blood calcium and phosphorus levels
“crush”
growth plate or physis
go away when we stop growing
transverse cartilage plate
this grows bone by extending from the bone toward the joing which is turned into bone
normal joints
Fibrous – No joint space, and NO MOVEMENT! (skull bones)
Cartilaginous – no space between, and limited movement (vertebral bones, wrist bones)
Synovial – joint bones by ligaments, have joint space, allow great range of motion (knee, elbow, shoulder, wrist and hip, etc.
synovial joints
- Contain a space and synovial fluid
- Contain a plate of cartilage – buffer for shock and wear
- The movement of tissues around joints is smoothed by bursae, which are small sacs lined by synovial cells that secrete the lubricating fluid.
These are between tendon and bone or between skin and bone (the elbow)
osteoid
unmineralized bone
network of bone matrix protein fibers
osterocytes
“bone cells”
comprise about 90% of all bone cells, linked to one another by cytoplasmic extensions that run through tiny channels called canaliculi
Type I muscle fibers
slow twitch, designed for sustained action and plentiful in mitochondria (gives them a darker coloring)
type II muscle fibers
fast twitch, designed for short bursts of intensity and have fewer mitochondria (gives them lighter coloring)
achrondroplasia
- Genetic syndrome of short-limbed dwarfism caused by failure of the epiphyseal cartilage to form normally.
- Normal sized trunk attached to short arms and legs.
- Other features: face is small compared to skull, saddle nose, small jaw, bowed legs, and sway-back posture (lordosis)
ganu varum / Genu Valgum
abnormalities of spine curvature
- Kyphosis – abnormal forward curvature
- Lordosis – abnormal backward curvature (pregnant or elderly)
- Scoliosis – abnormal lateral bending
pregnancy=increased lordosis due to increased anterior load
osteogenesis imprefecta
“brittle bone disease”
- Disorder of bone maturation
- Spectrum of inheritable disorders caused by genetic defects in collagen formation
- too little bone tissue (brittle bone disease)
- Bones easily fractured
- Defective middle-ear bones (deafness), defective collagen, abnormal tooth development, floppy heart valves, thin sclera (appears blue)
Pagets disease
- Different than Paget disease of the skin
- This is where bone remodeling is defective
- Possible viral etiology
- Increased osteoclast (bone crush!) activity – breaks down bone and stimulates new bone formation by osteoblasts.
- Usually femur, pelvis, spine
- Usually asymptomatic
- Elevated alkaline phosphatase (AP) – enzyme needed for osteoclast activity
- Can treat with bisphosphonates to suppress osteoclasts
osteoporosis
- Acquired condition of decreased mineralization of bones, increased bone porousness and decreased bone mass to the point that the bone can no longer provide proper support and strength.
- Primary = most common, post-menopausal women
- Secondary = caused by another condition (hyperparathyroidism, etc.)
Signs/Sx:
- most are asymptomatic until a fracture occurs
- Significant health/financial burden for these fractures
- Usually vertebra, femur, pelvis and wrist fx from falls
- Sequelae = pneumonia and death
osteomalacia
- “soft bones” – defective mineralization (calcification) of bone protein fibers
- Uncommon, qualitative defect. Normal number of osteocytes, but they do not mineralize properly.
- Most due to: calcium, phosphate or vitamin D issues (poor intake or malabsorption)
- Meat + dairy are main dietary sources of Ca++ and phosphate.
- Crohn’s disease can interfere with Ca++ and Vit. D absorption
- Signs/symptoms: skeletal deformities (rickets – from vitamin D deficiency)
- Diagnosis/treatment: radiologic findings are subtle. Treat with oral Ca++, Vit. D, phosphate
fractures
- closed: bone has not broken through skin
- open: bone protrudes through skin
- comminuted: multiple fractures in a single site
- greenstick: bend or break partially usually in children’s bones which are more flexible
- impacted: sudden end to end force that causes bone to collapses on itself
- compression: same as impact but vertebrae
- spiral: twisting force
- pathologic: results from disease that weakens bone locally so fracture happens b/c of normal stress
osteomyelitis/ acute osteomyelitis
bacterial bone infection
Microorganisms grow →increase pressure in bone →ischemia and vascular compromise
Infection spreads through bone → cortex devascularization and necrosis
patient presents very ill
s/s:
- Fever
- Night sweats
- Chills
- Restlessness
- Nausea
- Malaise
- Drainage (late)
osteomyelitis
bacterial bone infection
Microorganisms grow →increase pressure in bone →ischemia and vascular compromise
Infection spreads through bone → cortex devascularization and necrosis
chronic osteomyelitis
- Infection lasting longer >1 month or has failed to respond to initial course of antibiotic therapy
- Continuous and persistent or process of exacerbations and remissions
- Systemic signs diminished
- Local signs of infection more common
◦Pain, swelling, warmth
• Granulation tissue turns to scar tissue → avascular → ideal site for microorganisms to grow → away from antibiotic penetration
they don’t present as acutely ill
labs in MSK disease
(inflammatioN) ESR: inflammation anywhere in the body
CRP: inflammation anywhere in the body
(bone disease)
Alkaline phosphatase: osteomalacia, bone tumors/mets, paget disease of the bone, hyperparathryoidism
Rheumatoid factor: positive in about 70% of patients with RA, can also be + due to other autoimmune diseases
CK: myositis, myopathy, trauma; can also be high due to muscular exertion, seizures, heat stroke, myocardial infarction
osteoarthritis
- Degenerative joint disease
- Primary = Progressive NON-INFLAMMATORY erosion of joint cartilage
- Tends to occur in the DIP joint (heberden nodes)
- Increases with each decade of life
- Mainly weight-bearing joints (hip, spine, knee)
- Secondary = from abnormal stress (obesity, jack hammers, physical malformations, diabetic peripheral neuropathies)
increased wear and tear!
activity related joint pain that is relieved by rest
joint may have crepitus
Rheumatoid arthritis
- autoimmune, chronic, systemic
- 1-2% of population is affected
- intense inflammation in joins
- unknown etiology, possibly viral, familial tendency
- z deformity in hands
- rheumatoid nodules
- early morning joint stiffness and pain
- can affect other tissues- heart, blood vessels, eyes, skin, lungs, skeletal muscles
- usually affects joints symmetrically
- treatment is more aggressive now, to stop destruction in its tracks
ankylosing spondylitis
- Chronic relapsing arthritis that primarily affects joints of the vertebral processes in the spine.
- Usually affects the SI joints
some patinets with severe chronic inflammatory disease, including RA may develop second
gout
- Signs/Symptoms: severe inflammation, tenderness, may get renal colic from obstructive uric acid stones.
- Diagnosis:
- Clinical
- Fluid aspirate for crystal analysis
- Treatment includes:
- Dietary modification (avoid purines)
- Avoid alcohol
- Medications that increase renal uric acid excretion.
80% = men Great toe affected 90% of the time Primary – chronic metabolic disease associated with high uric acid levels, joint deposits of uric acid, and inflammatory, nodular subcutaneous deposits (tophi).
•Uric acid – sharp, cause inflammation, causes acute and chronic relapsing arthritis. Kidneys excrete this. Secondary – other causes. •Renal failure = can’t get rid of the uric acid, or increased production in patients from other causes (malignancies, etc.)
acute septic arthritis
- Most common in adults = staph aureus, streptococci, H. flu., Neisseria gonorrhea (most common in young, sexually active adults), E. Coli, TB, Salmonella, Brucella, etc.
- Most patients are on steroids, IVDU, or have infected IV lines or catheters
- Patients with RA are at risk
- Can happen in kids with AOM or other infections
- Diagnosis = clinical
- Treatment = antibiotics
tendinitis
•inflammation or pain in a tendon
tenosynovitis
- inflammation or pain of synovial sheath through which the tendons slide
- Elbow, wrist, shoulder, and knee are common
Tennis elbow (lateral epicondylitis)
•ligaments that attach forearm extensor muscles to the lateral epicondyle of the humerus
shin splints
•pain and tenderness along the anterior aspect of the tibia where muscle attaches
bursitis
- inflammation of the bursa (inflamed, fluctuant mass
- Treatment: rest, NSAIDs, surgery rarely necessary
carpal tunnel syndrome
condition of the tendons and tendon sheaths of the ventral wrist in persons doing repetative finger/wrist motions
tinels and phalens test
rhabdomyolysis
Rhabdomyolysis releases myoglobin:
◦Secondary to something else (burns, heat stroke, alcoholic binge drinking, crush injury, muscle contractions during seizures, drug overdose, poisoning, electrical shock)
◦Myoglobin is cleared by the kidneys
◦Muscles are swollen, tender, weak
◦Urine can be brown
◦May develop renal failure and require dialysis! L
Myasthenia Gravis
Uncommon, acquired autoimmune disease of neuromuscular junction
- Antibodies attach to acetylcholine receptors on the muscle side of the synapse, blocking acetylcholine released from the motor end plate (thus interrupting the nerve impulse)
- No sensory or autonomic component
- Thymic hyperplasia or thymoma present in most patients; mechanism obscure
- Signs/Symptoms: usually women 20-40 years old, older men, drooping eyelids or double vision (eye muscle weakness), slack facial muscles (difficulty chewing), then it progresses proximally and can affect all muscles
- Diagnosis: measure blood acetylcholine receptor (AChR) antibody levels, electromyography.
- Treatment: symptomatic, removal of antibody by plasmapheresis, removal of thymus
Myasthenia Gravis
Uncommon, acquired autoimmune disease of neuromuscular junction
- Antibodies attach to acetylcholine receptors on the muscle side of the synapse, blocking acetylcholine released from the motor end plate (thus interrupting the nerve impulse)
- No sensory or autonomic component
- Thymic hyperplasia or thymoma present in most patients; mechanism obscure
- Signs/Symptoms: usually women 20-40 years old, older men, drooping eyelids or double vision (eye muscle weakness), slack facial muscles (difficulty chewing), then it progresses proximally and can affect all muscles
- Diagnosis: measure blood acetylcholine receptor (AChR) antibody levels, electromyography.
- Treatment: symptomatic, removal of antibody by plasmapheresis, removal of thymus
diaphysis (bone anatomy)
long, slender middle part that joints the distal parts
metaphysis (bone anatomy)
from the growth plate down toward the diaphysis
pons
(brainstem)
Associated with sleep, respiration, swallowing, bladder control, facial movement and sensation.
medulla oblongata
(brainstem)
Control center of heart and lungs.
midbrain
Associated with vision, hearing, motor control, alertness.
thalamus
Relay sensory and motor signals to cerebral cortex, regulate consciousness
-Hypothalamus: Link nervous system to endocrine system.
gray matter
neuronal cell bodies
white matter
glial cells, myelinated axons
PATHWAYS
CSF
indicated for suspected meningitis, hemorrhage, leukemic infiltration of meninges, and some neoplastic disorders
if increased ICP suspected, further assessment obtained because lowering spinal pressure may cause downward herniation of cerebellar tonsils
note:
pressure: increased pressure indicates increased ICP
color: bleeding associated with disease is characterized by uniformly colored CSF
cells: presence of few lymphocytes, RBCs, or neutrophils can be abnormal. purulent meningitis is associated with very high neutrophil counts
protein: increased protein is usually a sign of infection, inflammation, degenerative disease or hemorrhage
glucose: low glucose CSF level may reflect bacterial or fungal infection
cranial nerves
spinal cord
C1-8
T1-12
L1-5
8am breakfast, 12pm lunch, 5pm dinner
epidural hematoma
accumulation of blood between the skull and the dura matter
almost always caused by a skull fx that tears the middle meningeal artery (MCA)
bleeding is rapid- ARTERIAL
forces tentorial herniation
“lucid interval”
initial trauma is a concussion severe enough to render the patient unconscious, they regain consciousness before becoming unconscious again
subdural hematoma
accumulation of blood between the dura and arachnoid caused by relatively slow venous bleeding
can be mild trauma
anticoagulant use, falls, assaults, car accidents, athletic trauma
shaken baby syndrome
hydrocephalus
accumulation of excess CSF
obstructed flow= obstructed or non-communicating
impaired resorption = communicating
normal pressure hydrocephalus can occur, in adults and is usually due to impaired CSF absorption
spontaneous subarachnoid hemorrhage
usually from a berry saccular aneurysm
thunderclap HA- sudden onset of severe HA
meningitis
most common: bacterial or viral but can be fungal
purulent meningitis is caused by aerobic bacteria:
Ecoli, haemophilus influenza, streptococcus pneumoniae, neisseria meningitdis
viral may be “aseptic meningitis” since bacterial cx are negative
viral= lymphocytes, normal glucose
bacterial=neutrophils, low glucose
multiple sclerosis
demyelinating disease
autoimmune
onset usually 18-40 years old
Lou Gehrigs disease
- Degenerative condition of motor neurons in the gray matter of cerebral cortex, brain stem and spinal cord.
- Familial = 10%
- Average age of onset = 55, familial = 35-45
- Weakness, atrophy, muscle twitching then speech, locomotion and respiratory issues
- COGNITION and SENSORY FUNCTIONS are usually UNIMPAIRED!
- Death = respiratory failure.
- Dx: clinical
- Treatment = supportive
Huntingtons disease
- Autosomal dominant – causes neuron degeneration in the basal ganglia
- Most cases are inherited. More common in white populations. Some cases d/t spontaneous mutations
- Asymptomatic until adult life (20-40 yrs), so an adult with the defect has often had children.
- Early signs = subtle personality changes, restlessness, uncoordinated body movements.
- Later signs = dementia, involuntary, writhing movements called “chorea”
- Relentlessly progressive and fatal (usually 10-20 years after symptom onset).
- Diagnosis = genetics and genetic counseling for relatives.
- Huntington’s Chorea video: https://www.youtube.com/watch?v=JzAPh2v-SCQ
bells palsy vrs. CVA
decorticate vrs decerebrate
corneal abrasion
scratch on cornea
very painful
hyphema
hemorrhage into anterior chamber
can cause blindless
ocular emergency
proptosis
forward displacement of the globe from orbital fx
presbyopia
~age 40, inability to focus on near objects and hold reading materials farther away (natural part of aging)
focusing power gradually lost over the years
myopia
nearsightedness
elongated globe
hyperopia
farsightedness, foreshortened globe
astygmatism
dysfunctional cornea
conjunctivitis
mild, common, and usually bacterial, viral, or allergic, chemical
contangious until 24 hours of antibiotics if bacterial
purulent discharge=bacterial
if herpetic, steroids will worsen! caution
use soap and water
incubation 5-10 days and commonly spreads to other eye
conjunctivitis
mild, common, and usually bacterial, viral, or allergic, chemical
contangious until 24 hours of antibiotics if bacterial
purulent discharge=bacterial
if herpetic, steroids will worsen! caution
use soap and water
incubation 5-10 days and commonly spreads to other eye
sty
localized inflammation, sometimes small abscess of the eyelid resulting from bacterial infection of sebaceous glands in the eyelid
chalazion
local inflammatory reaction of sebaceous glands, long lasting condition characterized by chronic granulomatous inflammation
blepharitis
diffuse inflammation of the eyelid
dacryocystitis
inflammation of lacrimal apparatus
clogged tear duct
keratoconjunctivitis sicca
chronic dry eyes that is usually attributed to insufficient tear formation
can be part of sjogren syndrome
subconjunctival hemorrhage
bleeding under the conjunctiva, alarming to patients
white sclera becomes red
self limiting
pterygium
less common than pinguecula, larger, and shaped like an insect wing
yellowish fibrovascular tissue that grows in the sclera on either side as result to sun exposure
pinguecula
most common and is usually seen as a small lump on the nasal side of the cornea in an elderly person
yellowish fibrovascular tissue that results from sun exposure
arcus senilis
white arc of lipid depositied around the edge of the cornea
keratitis
inflammation of the cornea
any infectious agent can be responsible
no steroids until dx is clear incase of herpesvirus infection
keratoconus
cone-shaped cornea instead of spherical cornea
cataract
clouded lens, age related degeneration of lens fibers, attracts more water into the lens
uveitis
Uveitis—inflammation of the uveal tract
◦Anterior (iritis and iridocyclitis)
◦Acute: idiopathic, trauma, surgery, Chlamydia, virus
◦Chronic: other autoimmune disease, herpes, syphilis, sarcoidosis, sympathetic ophthalmitis
◦Posterior (choroiditis)
◦Any of above plus diabetes, opportunistic infection
◦
Uveitis can have SERIOUS CONSEQUENCES including blindness!
retinal detachement
Retinal detachment causes blindness – this is a MEDICAL EMERGENCY!
◦With or without tears
◦Usually loss of part of the field of vision, floaters or flashes of light
◦Treatment: surgical repair!
glaucoma
optic nerve damage
usually associated with ocular HTN
usually increased intraocular pressure
optic disc in enlarged, cupped, pale
leading cause of blindness in the US
silent
open-angel: normal anatomy, dm risk factor, asymptomatic besides progressive loss of peripheral vision
closed angel “acute-angle” acute eye emergency, treatment must occur within 24-48 hours to avoid blindness (shallow anterior chamber)
severe eye pain, tearing, resness, blurred vision, and puffy eyelids
must see eye specialist STAT
acute otisis media
infection in the middle ear
Acute otitis media is a common infection in children.
◦Can be viral or bacterial
◦Usually secondary to viral URI
◦Anatomic and physiologic (Eustachian tube is narrow and more horizontal in peds, and immune system is immature)
◦Ear pain, fever, TM is bulging, red, dull. Loss of light reflex. Most cases (~80% self-limiting in a few days. AAP now recommends watchful waiting.
◦Complications: TM rupture, chronic otitis media, septicemia, meningitis, mastoiditis
chronic otitis media
Chronic otitis media is associated with hearing loss and complications.
◦Persistent (> 6 weeks), suppurative drainage into auditory canal through perforated TM. Hearing loss is common, speech impairments for children.
◦Should see ENT for management
cholesteatoma
Cholesteatoma – accumulation of keratin in middle ear – not a neoplasm.
◦Requires surgical removal, antibiotics
◦Tend to recur
◦Tympanostomy tubes may be helpful
vertigo
symptom not DX
false sensation of movement
presence of nystagmus=true vertigo
manieres disease
triad of vertigo, fluctuating hearing loss, and tinnitus x 12 hrs or so.
- Unknown etiology, likely from increased fluid in vestibular apparatus and cochlea.
- Nystagmus usually present.
- Treatment – low-salt diet, diuretics, refer to ENT!
- Epley Maneuvers - https://www.youtube.com/watch?v=9SLm76jQg3g
hearing loss
- About 10% of US population has some degree of deafness.
- Conductive – interferes with transmission of sound to TM or beyond. Impacted cerumen, chronic otitis media, perforated TM.
- Sensory – issue with cochlear conversion of vibrations into sensory nerve signals. Noise trauma from work, prolonged exposure to loud music, genetics, ototoxic drugs.
- Neural – issue with sensory nerve signals or lack of integration into the consciousness. Neuroma, demyelinating disorders (MS), CNS trauma.
- Sensory and neural are often lumped together as sensorineural hearing loss!
nodular xanthoas
deposits of cholesterol that tend to occur knuckles, elbows, and knees
butterfly rash
erythematous macules from a butterfly rash on the cheeks and across the bridge of the nose
SLE
sarcoidosis
violaceous, confluent plaques
sunburns
superficial=erythema only
partial thickness=burns with blisters
chronic exposure=photo-aging
impetigo
contangious
superficial
staph or strep
honey colored crusts
tx: topical or oral antibiotics
ringworm
tinea species fungi
topical antifunals
molluscum cantagiosum
common, self limited contagious viral disease caused by pox-virus
lesions often occur near genitals, face, lips, and eyelids
small, firm, dome-shaped flesh-colored nodules a few mm in diameter
eczema
acute inflammatory rxn of skin
itchy, red, weepy, crusted, red lesions
atopic eczema, common type I hypersensitivity
incredibly pruritic
worse in winter months
allergic contact eczema
delayed-type immune reaction (type IV hypersensitivity)
common with hapens (small protein antigens)
stimulates t cell reaction
poisen ivy, nickel, gold jewlery
erythema multiforme
- Acute, self-limiting reaction (type II hypersensitivity) in which an antibody attacks cells in the basement membrane of the epidermis.
- Fairly common!
- Lips and palms of children or young adults
- Can be an auto-immune reaction stimulated by herpes infection
- Drugs and vaccines are also responsible
- Can use systemic antiviral therapy
stevens-johnson syndrome
- SJS – if < 10% of skin surface is involved
- TEN – if > 30% of skin surface is involved
- Most cases are from drug hypersensitivity (especially sulfa or anti-seizure meds)
- Unknown mechanism, but could be a hapten reaction (similar to poison ivy)•Begins as fever, then skin lesions 1-2 weeks after exposure
Epidermal blisters, progress to necrosis and denuded skin.
- Lesions coalesce and produce skin damage similar to burns.
- Risk for fluid management issues and infection!
- TEN – manage inpatient on burn unit.
psoriasis
- Acquired, proliferative disease of the epidermis
- Epidermal hyperplasia that forms salmon-colored, dry, scaly, sharply delineated plaques
- Affects 1-2% of the US population
- Bilateral lesions! (elbows, knees, knuckles, but can spread to lower back, scalp, cleft between buttocks, nails)
- Unknown etiology, strong genetic component.
- Possibly auto-immune - 10-25% of cases will have an accompanying arthritic component.
- Diagnosis: clinical
- Treatment: topical tar, steroids, UV light therapy, and things that slow cell reproduction (chemotherapy, immunomodulators)
Erythema nodosum
- Acute disease
- Possible autoimmunity
- Red, extremely tender nodules of chronic inflammation on the anterior aspect of lower legs
- Adult women
- Most common associations:
- Infections (strep infection, TB)
- Medications (sulfanomides, OCPs)
- Illnesses (sarcoidosis, IBD, some CAs)
- Presentation: fever, tender nodules
- Diagnosis: clinical, sometimes biopsy
- Treatment: Supportive, self-limiting (few weeks)
pemphigus
- Rare, serious blistering disease
- Autoimmune antibody
- Middle-aged adults, Mediterranean heritage
- Skin and oral mucosa can be affected.
- Fluid accumulates, forms blisters, then they rupture to form weeping, crusted, inflamed patches.
- Usually trunk, face, neck, scalp (spares extremities)
- Huge risk for infection
- Diagnosis: clinical
- Treatment: Immunosuppressants
porphyria
- Group of inherited disorders of porphyrin metabolism.
- Porphyrins are pigments found in hemoglobin and myoglobin
- Signs and symptoms: abdominal pain, neurologic defects, skin lesions (including urticarial), and sub-epidermal blisters (worsened by sunlight).
vitiligo
- Common, acquired disorder characterized by white macules that can coalesce into large patches of white depigmented skin.
- Melanocytes are absent in affected areas
- Usually starts around age 20, but can affect any age•DM, Addison’s disease, thyroiditis, pernicious anemia, and head trauma are associated.
- Unknown etiology – autoimmune reaction is suspected (other autoimmune disorders are usually also present)
- Systemic phototherapy can stimulate cosmetic repigmentation
melanocytic nevi
- Pigmented mole
- Acquired benign tumor of melanocytes
- Usually appear before age 20
- Brown papule < 1 mm in diameter and slowly enlarge and become darker
- Usually stop < 5 mm
- Clear relationship between sun exposure, development of nevi, and development of malignant melanoma.
- Some removed for cosmetic reasons
- Dysplastic nevus – usually larger (6-15 mm), surrounded by a collar of irregularly pigmented skin.
- Premalignant – do not always become malignant.
Actinic (solar) keratosis
- Very common!
- Early precancerous forerunner of the SCC
- Small (< 1 cm), discrete, rough, scaly patch or thickly cornified nodule on sun-exposed skin (face, back of hand, back of neck)
- Common if light-skinned
- Can progress to invasive squamous carcinoma.
- AKs can be removed by superficial methods (curettage, lasering, topical chemo, cryotherapy)
