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
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
glucagon / glycogen / insulin metabolism
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
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
horseshoe kidney
single fused kidney
abnormal embryogensis
often seen in pts with turner syndrome
varicocele
scrotal varicose veins
scrotal enlargement and possibly infertility
tx: possible surgery
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)
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
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
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
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
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
bells palsy vrs. CVA
decorticate vrs decerebrate
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
astygmatism
dysfunctional cornea
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
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
keratoconus
cone-shaped cornea instead of spherical cornea
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!
butterfly rash
erythematous macules from a butterfly rash on the cheeks and across the bridge of the nose
SLE
