Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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
|