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80 Cards in this Set

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Chronic Reflux/Barrett's Esophagus
Esophageal epithelium (stratified squamous) metaplasia to gastric epithelium (simple columnar)
Dysplasia may be present
Inflammation, scarring, dysphagia
Pernicious Anemia
VitB12 malabsorption leading to insufficient RBC synthesis
Can stem from a problem with Intrinsic Factor (IF) synthesis or a deficiency in Vitamin B12
Can also be caused by AutoAb preventing binding of B12 and IF
Prader-Willi Syndrome
will have eleveted levels of Ghrelin, stimulating hunger in the hypothalamus
Acute gastritis
Can be caused by alcohol, anti-inflammatory drugs, stress
Chronic gastritis
Can be caused by:
Chemical - EtOH, reflux of bile into stomach
Autoimmune
Infection - Helobacter pylori
Helobacter pylori
causes chronic gastritis by attaching to surface epithelium and interfering with the formation of the gel-coat --> loss of protective layer. This causes inflammation, acid-induced ulceration and necrosis, and fibrous scarring. An obstruction can occur due to scarring at the lower esophagus or pylorus. At end, the effects of H. pylori can lead to hemorrhage or perforation
Zollinger-Ellison syndrome
hyperplasia of fundic stomach, gastrin-secreting tumors (gastrinomas)
high HCl secretion
inactivates pancreatic lipases --> diarrhea, steatorrhea
gastric ulcers
Malabsorption syndromes
deficits in absorption of fats, proteins, carbs, salts, or water
some causes:
brush border enzyme abnormalities
defective bile secretion
abnormal pancreatic enzyme secretion
Gluten enteropathy (celiac disease)
Immune-mediated inflammatory disease of small intestine
Atrophy and flattening of intestinal villi, hyperplasia of intestinal glands
Results in malabsorption syndrome from loss of SA
Diverticular Disease
High intralumenal pressure (possibly due to low residue diet) and weakened muscularis results in herniation of mucosa through weakened muscularis
Complications include inflammation, perforation, and hemorrhage
Crohn's Disease
Chronic inflammatory disease of unknown etiology affects small intestine (mainly terminal ileum) but may also affect colon
Patchy distribution w/ normal segments btw
Domed areas of edematous mucosa and submucosa w/ fissured ulcers and granulomas
Inflammation may be transmural and can lead to fibrosis and obstruction
Predisposes to cancer
Ulcerative colitis
unknown etiology, affects colon especially rectum
Acute phase characterized by inflammation w/ neutrophils accumulating in lamina propria and crypts forming abcesses of pus
Superficial ulcers w/ normal mucosa projecting above ulceration (inflammatory pseudopolyps)
Inflammation rarely transmural
High incidence of dysplasia and adenocarcinoma in chronic cases
Colon polyps (adenomas)/adenocarcinoma
Benign adenomas, varying degrees of dysplasia
tubular, tubulovillus, villus (most potential for neoplasia)
Adenocarcinoma: sigmoid colon most frequent site, malignant
Appendicitis Stages
Acute inflammation w/ surface ulceration and exudates
Spread through layers and into peritoneum
Peritonitis of right iliac fossa
If perforates, widespread peritonitis
Anosmia
loss of olfaction
Bitemporal hemianopsia
loss of lateral (temporal) visual fields in both eyes
can be caused by pituitary tumor
Ipsilateral nasal himianopsia
loss of medial (nasal) visual field on one side
can be caused by internal carotid aneurysm
Contralateral homonymous hemianopsia
lesion of the optic tract causing loss of lateral (temporal) visual field same side, medial (nasal) visual field opposite side.
results in loss of either left or right visual fields.
Papilledema
bulging of the optic disc
usually caused by an increase in cranial pressure (CSF)
Horner's Syndrome
injury to sympathetic trunk in neck
partial ptosis due to loss of tarsal muscle innervation
miosis (pupil constriction)
enopthalmos (retraction of eye)
Ipsilateral anhidrosis
Vasodilation
Strabismus
inability to direct both eyes towards same object
Diplopia
double vision
Lesion of CN VI causes
paralysis of LR --> strabismus and diplopia. Pt compensates by turning head so object is brought into alignment w/ affected eye
Lesion of CN IV causes
paralysis of SO, weakness of downward medial gaze (intorsion) most noticeable when going down stairs. Pt compensates by tilting head towards unaffected side. Should consider DDx of torticollis (lesion of XI)
Torticollis
lesion of CN XI
Oculomotor opthalmoplegia
lesion of entire CN III
Eye moves down and out, strabismus
Ptosis due to loss of innervation to levator palpebrae superioris m. (pt compensates by raising frontalis muscle, wrinkled forehead)
Dilated pupil b/c CN III carries parasympathetic innervation for constrictor pupillae m (leaving dilator pupillae to rule over iris tone)
Lack of accommodation
Stye
an infection in the ducts of the eyelids sebaceous glands which empty directly onto the surface of the eye
Chalazion
blockage of tarsal glands leads to inflammation on inside of eyelid
ptosis
drooping of the upper eyelid, aka "lazy eye"
miosis
pupil constriction
anhidrosis
lack of sweating
a lesion in CN IV will present as
eye will be extorted (lack of intorsion from Superior Oblique)
a lesion in CN VI will present as
eye will be adducted (lack of abduction from Lateral Rectus)
a lesion in CN III will present as
eye will be down and out
ankyloglossia
aka tongue-tie
insufficient cell degeneration under tongue during development
microglossia
small tongue
macroglossia
large tongue
macrostomia
"big mouth"
insufficient fusion of maxillary and mandibular processes at labial commissure
microstomia
"small mouth"
excessive fusion of maxillary and mandibular processes at labial commissure
bifid or forked tongue
results from incomplete union of 2 lateral lingual swellings
Diabetes Insipidus
Chronic renal disease caused by genetic defects in receptors for ADH or nonresponsive receptors for ADH
Results in hypotonic urine (increased water --> dilution)
Dwarfism
caused by decreased GH
Gigantism
caused by increased GH in children*
Acromegaly
caused by increased GH in adults*
Prolactin-secreting tumor symptoms
anovulation in females
decreased libido
infertilitiy
galactorrhea in males
Cretinism
congenital absence of the thyroid leading to profound neurological damage
Graves Disease (Hyperthyroidism)
Autoimmune antibodies to TSH receptors mimic* TSH leading to chronic activation
Presents with enlarged thyroid (goiter), exopthalmos, tachycardia, and fine finger tremors
Hypothyroidism
-Congenital hypoplasia of pituatary: decreased cell metabolism, mental lethargy, hypothermia, myxedema
-Hashimoto's disease: autoimmune antibodies to Tg --> destruction of thyroid follicles
-Insufficient dietary iodine
Hashimoto's disease
a type of hypothyroidism where autoimmune antibodies attack Tg leading to destruction of thyroid follicles
DO NOT CONFUSE w/ GRAVES DISEASE
Hyperparathyroidsim/Hypoparathyroidism
Can be genetic mutation of chief cells, cells can't sense calcium levels which can lead to hyper or hypo
Benign adenomas of gland can cause hyperparathyroidism. Increased PTH causes increased bone demineralization and calcium excretion (lead to renal calculi)
Idiopathic hypoparathyroidism, tissues don't respond to PTH
Cushing's Disease
caused by ACTH-producing pituatary tumor
Overproduction of cortisol leads to fat redistribution and muscle wasting as wells as immunosuppression
Increased androgens
Cushing's Syndrome
caused by functional tumor of adrenal cortex
Addison's Disease
chronic destruction of cortex caused by autoimmune responses or TB
Increased ACTH levels due to cortisol deficiency
Hypotension, muscle weakness, increased skin pigmentation
Diabetes mellitus : Type 1 (juvenile)
Insulin dependent
Autoimmune destruction of B cells, absent or deficient insulin secretion
~90% are juvenile (but can occur in adults)
Diabetes mellitus : Type II (adult-onset)
Insulin independent
Genetic predisposition
Insulin levels can be normal or elevated
Insulin resistance of peripheral target tissues may be due to increased number of insulin receptors or deficient signaling of GLUT4 transporter
corpora arenacea
aka brain sand
increases w/ age
is the precipitation of calcium phosphates and carbonates on carrier proteins
Hemolytic disease of the newborn (eythroblastosis fetalis_
mother lacks D antigen (Rh-), first child is Rh+, mother is sensitized to D antigen and produces antibodies. If future children are Rh+, maternal antibodies to D antigen cross placenta and lyse infant's RBC
Anemia
decreased oxygen-carrying capacity of blood
decreased # of erythrocytes (decreased Hct)
Defective or deficient Hb
Sickle Cell anemia: genetic mutation of hemoglobin polypeptide
Polycythemia
increased erythrocyte count (increased Hct)
Hemophilia Type A
defective or deficient factor VIII
Hemophilia Type B
defective or deficient glycoprotein 1b-factor IX
Thrombocytopenia
decreased platelets
caused by decreased production or increased destruction of platelets
induced by drugs or autoAb to platelets or megakaryocytes
Thrombocytosis
increased platelets (increases probability of thrombosis)
Neutrophilia
An increase in circulating neutrophils, caused by:
Epinephrine - transient, due to dilation of capillaries and release of neutrophils from marginating compartment
Glucocorticoids - increases mitosis
Infection - increased # of immature neutrophils released from bone marrow (clinically referred to as "shift to the left")
Band cells = immature neutrophils which have a curved, rod-shaped nucleus
Metastatic cancers of blood cell formation
Bone marrow is a common site for blood-borne metastasis of malignant tumors
Carcinomas of the breast, lung, kidney, and thyroid most common
Tumors lead to destruction of trabecular bone and osteolytic deposits
Prostatic cancer stimulates growth of new woven bone with osteosclerotic deposits
Chronic Leukemia
neoplastic proliferation of more mature leukocyte precursors (cells more differentiated) allows for normal production of other WBCs, RBCs, and platelets
Acute Leukemia
proliferation of immature "blast" cells, more malignant since these precursors are early stem cells for other cell types
Tumor in floor of Fourth ventricle
may affect VI and VII: adducted eyes, total ipsilateral loss of VII motor
Acoustic Neuroma
affects VIII and VII: auditory and vestibular problems, total ipsilateral loss of VII function
Bell's Palsy
may be due to viral infection in facial canal before it exits stylomastoid foramen: ipsilateral facial paralysis
can't close eye --> crocodile tears due to lacrimal punctum falling away from eye
droop of angle of mouth
loss of nasolabial fold
eyebrow droop
buccinator paralysis causes food to lodge in cheek
Genetic storage diseases
Inborn errors of metabolism result in accumulation of metabolites in hepatocytes
Glycogen storage disease, lipidoses, mucopolysaccharidoses, haemochromatoses
Acute Hepatitis
may resolve or become chronic
due to toxins, drugs, virus
hydropic degeneration of hepatocytes, progresses to spotty necrosis with aggregates of inflammatory cells around necrotic hepatocytes (Councilman bodies)
Kupffer cells proliferate
Regeneration
Chronic Hepatitis
Viral, toxins, autoimmune
Classified according to how far it progresses (stage) and how active (grade)
Necrosis of hepatocytes, fibrosis
Cirrhosis
End stage of several liver diseases where there is hepatocyte loss
Regeneration nodules encased in CT
Disruption of architecture affects blood flow, bile flow
Liver cancer
Hepatocellular carcinoma - most common
Common site of secondary metastasis of other cancers
Gallstones
calculi, solid concretions of bile which attract calcium and salt deposits
Pancreatitis
May be acute or chronic
Release of pancreatic enzymes causing chemical peritonitis
Hemorrhage and necrosis of pancreas and surrounding tissues
Lymph node reactive hyperplasia
Lymph nodes enlarge due to infection
Follicular hyperplasia: if response is mainly humoral, nodules in outer cortex enlarge due to B cell proliferation
Parafollicular hyperplasia: T cell activation
Increased macrophage activity causes dilation of sinuses
Hodgkin's Lymphoma
Different subtypes, usually manifests first in lymph nodes but can spread to other lymphoid organs and bone marrow
Characteristic Reed-Sternberg cells: tumor cells that usually arise from activated T cells, but may also arise from B cells and macrophages. Different subtypes have different prognoses
Non-Hodgkin's Lymphoma
Most tumor cells arise from B cells
Usually manifests first in lymph nodes but may arise from any lymphoid tissue, very commonly arises from MALT