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168 Cards in this Set

  • Front
  • Back
Deposition of an extracell proteinaceous material
amyloidosis
Storage disorder, fills organ and die of failure
amyloidosis
Plasma cell malignancy
MM
Bence jones proteins
MM
Tongue affects with amyloidosis
covered in translucent papules, hemorraghic

can have papules of the lip too
hemodialysis associated amyloidosis
(hemodialysis can build up amyloid)

normal occuring protein not removed
deposists in joints and bones
carpel tunnel syndrome and cervical spine paint
TONGUE INVOLVEMENT
secondary amyloidosis
inflamm process (i.e. tb, osteomyelitis, or sarcoidosis)

liver, kidney, adrenal, and spleen affected but not heart
is secondary amyloidosis slow or fast acting
slow
tx for amyloidosis
colchicine, prednisone, and melphalan
how can amyloidosis affect the heart
cardiac failure, arrythmia, or renal disease
biopsies for amyloidosis
rectal and labial salivary gland biopsy
stains for amyloidosis biopsies
congo red and crystal violet
diagnosis of amyloidosis
serum electrophoresis to determine whether a monoclonal gammopathy exists so MM can be ruled out
prognosis of amyloidosis
cutaneous form--no impact on survival
systemic form--death from cardiac and renal failure
cause of death in lupus
renal disease
cause of death in diabetes
atherosclerosis, heart attack, renal failure
is there effective therapy for amyloidosis?
no
treat infectious agent
renal transplantation
vitamin A deficiency
infancy--blindness
later in life--night blindness
what can make vitamin A deficiency progress to blindness
ulceration occurring with dryness of skin and conjunctiva
another name for vit A
retinol
what is vit A important for
maintenance of vision
growth and tissue differentiation
another name for vit B1
thiamin
what is vit B important for
coenzyme for several metabolic reactions and proper functioning of neurons

(neural system!)
who do you see vit b1 deficiency in
alcoholics and due to diet (SE Asia)
cardio problems with vit b1 deficiency
peripheral vasodilation
heart failure
edema
neurologic problems with vit b1 deficiency
peripheral neuropathy
Wernicke's encephalopathy
early symptoms of Beriberi
loss of appetite
tingling hands and legs
numbness, aches, pains
weakness and wasting of leg muscles
difficulty in walking
infantile beriberi
cause--if breast fed by a vit B1 deficient woman
symptoms--fretful vomiting, weight loss, swelling, convulsions
another name for vit b2
riboflavin
what is vit b2 involved in
cellular red-ox reactions
vit B2 def signs
glossitis
angular chelitis
sore throat
swelling and erythema of the oral mucosa
seborrheic dermatitis
which vit def can have seborrheic dermatitis
vit b2 (riboflavin)
which vit def can have normocytic normochromic anemia
vit b2 (riboflavin)

--same affects as anemia (same oral findings--atrophic glossitis)
another name for Vit B3
Niacin
what is Vit B3 (niacin) responsible for
coenzyme for cellular red-ox reactions
what disease can occur with vit B3 deficiency
pellegra
what is pellegra
triad of...
dermatits
dementia
diarrhea
tongue vit b3 def symptoms
stomatitis
glossitis
symptoms of niacin def
pellegra
tremors and irritability
lethargy
mental depression, confusion, headache
loss of appetite
oral lesions
sources of niacin
meat, poultry, fish
mushrooms, whole grain, enriched breads and cereals
what can cause smooth tongue
vit deficiency
anemia
malabsorption
abx
another name of vit C
ascorbic acid
what is vit c necessary for
proper synthesis of collagen
sympt of vit c deficiency
scurvy
wound healing delayed and wound breakdown
(childhood) painful subperiosteal hemorrhage
osteomalasia
Vit D deficiency
weak fragile bone structure (osteoid without sufficient calcium to mineralize completely)
vit D
considered a hormone
sunlight essential
cereal and milk fortified
calcium absorption in the gut
rickets
vit D deficiency
irritability, growth retardation and prominence of costochondral junctions
bowing of legs due to poor mineralization of skeleton
Rachitic Rosery
enlargement of costochondral junction
(rickets--vit d def)
vit K
fat soluble
necessary for proper synthesis of various proteins including clotting factors 2, 7, 9, and 10
what can happen with vit k def
malabsorption syndromes or microflora elimination with abx
oral anticoagulants (dicumarol) inhibit normal ezymatic activity
oral effects of vit k def
gingival bleeding intraorally
what is the coagulopathy in vit k def related to
inadequate synthesis of prothrombin and other clotting factors
anemia
a reduction in the oxygen carrying capacity of blood
nutritional anemias can be a result of
iron def, folic acid, b 12
oral manifestations of anemia
skin and mucosal pallor
angular chelitis
erythema and atrophy of oral mucosa
loss of filiform and fungiform papillae on dorsum of tongue
iron def anemia can be a result of
def of iron intake
blood loss (menstrual or internal bleeding)
poor iron absorption
inc requirement for iron (pregnancy)
iron def anemia definition
insufficient amount of iron available in bone marrow for RBC dev
iron def anemia symptoms
asymptomatic
weakness, fatigue
mucosal pallor
erythematous, smooth, painful tongue
low hemoglobin content, reduced hematocrit
% of women with iron def anemia
20%
symptoms of iron def anemia
fatigue, easy tiring, palpatations, lightheadedness and lack of energy
IDA can be from
excess blood loss
inc demand for rbcs
dec intake
dec absorption
what can IDA predispose a person to
cadidiasis
glossitis
hypochromic microcytic RBC's in addition to reduced numbers
why are you more prone to candidiasis if you have IDA
your T cells aren't as healthy
tx for IDA
iron supplementation
response is prompt, usually normal in 1-2 months
Plummer-Vinson Syndrome
IDA in conjunction with glossitis and dysphagia
premalignant
associated with oral and esophagial SCC
burning sensation tongue and oral mucosa
angular cheilitis and smooth red DT
who does P-V syndrome usually affect
scandinavian women or N. european (30-50)
tx of P-V syndrome
correct the IDA
esophageal dilation
5-50% prevalence of CA
P-V syndrome symptoms
dysphagia
esophageal webs
koilonychea (spoon shaped nails)
hypochromic microcytic anemia
pernicious anemia
megablastic anemia caused by poor absorption of cobalamin (vit b12, extrinsic factor)
intrinsic factor made by parietal cells of stomach needed for vit b12 absorption
mechanism of pernicious anemia
dec level of intrinsic factor (which is secreted by parietal cells of stomach) needed for absorption of vit b12 which is transported across the intestinal mucosa by intrinsic factor
causes of pernicious anemia
AI
gastrectomy
gastric cancer
gastritis
what is b12 needed for
dna synthesis (without it, rapidly developing cells are affected--marrow, epi)
symptoms of pernicious anemia
weakness
pallor
fatigue on exertion
nausea
dizziness
headache
diarrhea
abdominal pain
weight loss
severe paresthesia--tingling and numbness of extremities
oral manifestations of pernicious anemia
angular cheilitis
mucosal pallor
painful, atrophic and erythematous mucosa
mucosal ulceration
loss of papillae on dorsum of tongue
burning and painful tongue
lab testing for pernicious anemia
low serum vit b12 and gastric achlorhydria
megaloblastic anemia
rbcs are immature, large, and have nuclei
tx of pernicious anemia
injections of b12, improves over time but all papillae may not regenerate

monthly injections of cyanocobalamin
why is absorption compromised with pernicious anemia
the lining of the stomach can only take up cobalamin-intrinsic factor complex (the vitamin cannot be absorbed unless both components are present)
why do most pts with pernicious anemia lack intrinsic factor
AI destruction of the parietal cells with decreased absorption of cobalamin
how often is the tongue affected in pernicious anemia
50-60% of the time
pituitary dwarfism
diminished production of growth hormone or reduced capacity of the tissues to respond to growth hormone
shorter than normal
body proportions appropriate
hyperpituitarism
excess hormone produced by ant pituitary gland
pituitary adenomas produce excess growth hormone
juvenile hyperpituitarism
gigantism
excessive growth (entire skeleton)
may exceed 8 feet in height and weigh several hundred pounds
headaches, chronic fatigue, muscle and joint pain
increased production of GH usually related to pituitary adenoma
gigantism
when does gigantism take place
before closure of epiphyseal plates
acromegaly
excess production of GH after closure of epiphyseal plates
pituitary adenoma
head and neck symptoms of hyperpituitarism
enlargement of nasal bones, maxilla, mandible
larger sinus (deep voice)
malocclusion, thickened lips, macroglossia
surgery to excise pituitary adenoma
adult hyperpituitarism
acromegaly

poor vision, photophobia, enlargement of hands, feets and ribs
what does excess GH (with acromegaly) cause
htn
heart disease
hyperhidrosis
arthritis
peripheral neuropathy
renewed growth of small bones of hands and feet and membranous bones of skull and jaw
acromegaly
age of onset to diagnosis/symptoms for acromegaly
9 years from symp to diagnosis with average age of onset 42
h&n affects of acromegaly
inc growth of mand with prognathism, apertognathia, spacing of teeth and macroglossia
tx of acromegaly
remove or treat adenoma
other complications with acromegaly
hbp
diabetes
CAD
CHF
colon cancer
resp disease
life span shortened
hypothyroidism
decreased output of thyroid hormone
cretinism
seen with hypothyroidism
characteristics of hypothyroidism
thickened lips
enlarged tongue
short stature
puffy face
cold intolerance
mental retardation
lethargy
primary hypothyroidism
thyroid can't produce amount of hormones pituitary calls for
secondary hypothyroidism
thyroid isn't being stimulated by pituitary to produce hormones
tx of hypothyroidism
thyroxine (aims to normalize serum TSH concentration)

always check for angina and perform an ECG
what can happen in an adult with dec thyroid levels for a long time
deposition of GAG ground substance in GQ tissues, producing a non-pitting edema

primary form: thyroid gland abnormal
secondary: pituitary gland does not produce enough TSH
myxedema
symptom of hypothyroidism

thick skin, puffy face
lethargic
cold intolerance
slow speech
excess production of thyroid hormone, increasing metabolism
hyperthyroidism
causes of hyperthyroidism
Graves disease (AI)
thyroid hyperplasia
benign and malignant thyroid tumors
pituitary disease
metastatic tumors
85% of cases of hyperthyroidism related to what
graves disease
graves disease
autoantibodies against receptors for TSH which seems to stimulate thyroid cells to release excess thyroid hormone
goiter
hyperthyroidism
what can make the eyes bulge in hyperthyroidism
GAGs depositing and building up behind the eyes
who/when does graves affect
3rd-4th decades
5-10x women
symptoms of graves
nervousness
heart palpitations
heat intolerance
emotionally labile and muscle weakness
ocular findings in hyperthyroidism
eyelid retraction and lid lag
exopthalmos (accumulation of GAGs in the retro-orbatal CT
appearance of hyperthyroidism
rosy complexion
erythema of palsm
heat intolerance
excessive sweating
fine hair
tachycardia
warm smooth skin
soft nails
irritability
nervousness
weight loss
exopthalmos
weight loss despite increased appetite occurs in
hyperthyroidism
what are many signs of hyperthyroidism related to
increased metabolic rate cause by excess thyroid hormone
diagnosis of hyperthyroidism (lab)
assay free T4 (thyroxine) and TSH levels
T4 should be elevated and TSH depressed
tx of hyperthyroidism
surgery
meds to suppress thyroid activity
radioactive ablation of thyroid tissue followed by lifelong admin of appropriate levels of thyroid meds
radioactive iodine
drug therapy that blocks use of iodine (propylthiouracil and methimazole)
surgery
what does PTH play a role in
ca and phos metabolism
what is a thyroid storm in uncontrolled hyperthyroisim
delirium, elevated temperature, and tachycardia
what is your jaw going to look like with hyperparathyroidism
bone is very osteoporotic looking, no trabeculae (NOT CGCG--differential is in radiograph, NOT histo)
what levels are elevated with hyperparathyroidism
blood calcium (hypercalcemia) and phosphorus (hyperphosphatemia)

-->these create altered bone metabolism
what is hyperparathyroidism
excessive secretion of parathyroid hormone by the 4 parathyroid glands
etiology of hyperparathyroidism
hyperplasia of parathyroid glands
benign adenoma of parathyroid gland
malignant parathyroid tumor
who does hyperparathyroidism typically occur in
middle aged adults, females
how does the parathyroid gland regulate the blood level of calcium
by its effects on the GI tract, kidney, and bone
primary
hyperparathyroidism
results from disease in the parathyroid gland(s)
secondary hyperparathyroidism
results from abnormal excretion of clacium by the kidneys
clinical manifestations of hyperparathyroidism
stones, bones, groans, and moans

kidney stones
bone and joint pain due to excess Ca mobilization
GI cramping due to excess Ca absorption
personality disorders
oral manifestations of hyperparathyroidism
well defined UL or ML RL in jaws
brown tumors of hyperparathyroidism
hyperparathyroidism is histologically identical to what
CGCG
brown tumors
hyperparathyroidism
radio features of hyperparathyroidism
mottle or granular appearance of bone
partial loss (effacement) of lamina dura

tooth mobility
diagnosis of hyperparathyroidism
performance of blood tests for serum Ca, P, and PTH levels
tx of hyperparathyroidism
dependent on whether the increased PTH levels are caused by tumor, kidney disease, vit D deficiency
what happens to bone lesions of hyperparathyroidism when the disease is successfully treated
they resolve
addison's disease
primary adrenal cortical insufficiency (insufficient production of adrenal steroids)
what can cause primary adrenal cortical insufficiency (with addison's disease)
idiopathic destruction of adrenal cortex (AI)
malignant tumor
tuberculosis
what occurs in response to the primary adrenal cortical insufficiency with addison's?
pituitary secretes ACTH to stimulate adrenal cortex
what is an additional SE of addison's disease
pigmentation from melanin secreting hormone

can happen especially in the palmer skin creases, nails, and gums
brown pigmentation (bronzing) of the skin
addison's disease
melanotic macules can develop on oral mucosa
addison's disease
tx of addison's
replacement steroid administration
hypercortisolism aka...
cushings syndrome
hypercortisolism
increased glucocorticoid levels with most cases
hypercortisolism is cushings if...
from adrenal or pituitary tumor
weight gain is where with cushings
central areas of the body

can get diabetes
buffalo hump
hypercortisolism
fat accumulation in dorsocervical spine
moon face
hypercortisolism
fatty deposition in facial areas
other findings of hypercortisolism
hirsuitism
red-purple abdominal striae
poor healing
osteoporosis
htn
mood changes
muscle wasting
weakness
diabetes mellitus
chronic disorder of carb (glucose) metabolism
high glucose levels (hyperglycemia)
three pathways of DM
lack of insulin
defective insulin that does not lower blood glucose
insulin resistance due to obesity
what happens when insulin is lacking due to DM
cells are starved of energy, tissues break down

breakdown of fat releases ketone acids (that lower blood pH so can cause ketoacidosis, lead to diabetic coma and death)
type 1 DM
insulin dependent diabetes
AI
diagnosis peaks around age 20
thin body build
3 P's of DM type 1 diagnosis
polydipsia (excess thirst)
polyuria (excess urination)
polyphagia (excess appetite)
type 2 DM
noninsuling-dependent
95% of diabetics
obesity increases
oral hypoglycemic agents
insulin dependent diabetes complications
eye
kidney
nerves
tx of type 2 DM
rigorous control of blood glucose (injections, diet, exercise)
insulin pump
clinical features of DM
accelerated atherosclerosis
impaired circulation
impaired transport of O2
ulceration
gangrene
htn
kidney failure
stroke
infections
oral complications of DM
most severe in those whose blood glucose is not well controlled (brittle diabetic)
fungal infections
candida albicans
mucomycosis
xerostomia (so inc risk for candidiasis and caries)
how does someone with DM respond to plague
heightened response

erythematous, hyperplastic gingiva
excessive perio, mobility
early tooth loss
slow wound healing
hypophosphatasia
hereditary dec in serum alkaline phosphatase
what is alkaline phosphatase important for
calcification of bone and cementum of teeth
what happens to cementum with hypophosphatasia
lack of or abnormal forms so premature loss of deciduous ant teeth
deciduous molars and permanent teeth not affected
systemic features of hypophosphatasia
bowing of the legs and bone fractures
what vit def with beriberi
B1
pellegra
niacin deficiency
plummer-vinson syndrome is IDA with...
glossitis and dysphagia
what cancers is p-v syndrome associated with
oral and esophageal SCC
weakened vascular walls, petechial hemorrhages, ecchymosis
survy