Green Flags Flashcards
(345 cards)
1
Q
active error
A
occurs at level of front line operator- wrong dose programmed in
2
Q
latent error
A
accident waiting to happen- having various pumps at the hospital
3
Q
root cause analysis
A
uses records and participant interviews to identify all the underlying problems that led to an error. Prince failure in the future
4
Q
failure mode and effects analysis
A
uses inductive reasoning to identify all the ways a process might fail and prioritize these by their probability of occurrence and impact on patients
5
Q
roll over, hands together, laughing
A
3 mo
6
Q
sit up , transfer cube, single syllables, self feed
A
6 months
7
Q
crawling, object permanence
A
9 mo
8
Q
stand/walk, block into cup, 1-3 words, drink from cup
A
12 mo
9
Q
walk backward, run, build 2 cube tower, 6 words, utensils
A
15 months
10
Q
stranger anxiety
A
6-12 mo
11
Q
seperation anxiety
A
12-15 mo
12
Q
climb stairs, kick ball, 4 cube tower, combine words, brush teeth
A
18 mo
13
Q
jump 6 cube tower, half understandable, wash and dry hands
A
2yr
14
Q
jump forward tricycle, copy circle, understandable, pour cereal, brush teeth, dress, play board games
A
3 y
15
Q
hop on one foot, copy a plus sign draw stick figure, clothes button, magical thinking
A
4y
16
Q
tie shows, copy square, triangle, identify colors, identify coins, count to five
A
5 yyear
17
Q
logical thinking
A
6 y
18
Q
gender identiy
A
3 years
19
Q
potty train
A
2-3 years
20
Q
1 std
A
68%
21
Q
2 std
A
95%
22
Q
3 std
A
99.7%
23
Q
cervical LN drain what
A
head and neck
24
Q
hilar LN drain what
A
lungs
25
mediastinal LN drain what
trachea and esophagus
26
axillary LN drain what
upper limb, breast, skin above the umbilicus
27
celiac LN drain what
liver stomach spleen, pancreas, upper duodenum
28
SMA LN drain what
lower duodenum, jejunum, ileum, colon to the splenic flexure
29
IMA LN drain what
colon from splenic flexure to upper rectum
30
internal iliac LN drain what
lower rectum to anus above the pectinate line, bladder, vagina, cervix, prostate
31
para-aortic LN drain what
testes, ovaries, kidneys, uterus
32
superficial inguinal LN drain what
anus below pectinate line, skin below umbilicus, scrotum, vulva
33
popliteal LN drain what
dorsolateral foot and posterior calf
34
right lymphatic duct drains what
right arm and face above the right diaphragm
35
thoracic duct drains what
everything but the right arm, face and chest drains into the left subclavian
36
hay fever, rhinitis, eczema, hives, asthma- HSN?
HSN1
37
acute hemolytic transfusion reaction
HSN2
38
bullous pemphigoid
HSN2
39
anaphyalxis
HS1
40
autoimmune hemolytic anemia
HSN2
41
SLE
HSN3
42
contact dermatitis
HSN4
43
Graft vs host
HSN4
44
MS
HSN4
45
polyarteritis nodosa
HSN3
46
myasthenia gravis
HSN2
47
goodpasture
HSN2
48
Graves
HSN2
49
GBS
HSN2
50
poststep glomerulonephritis
HSN3
51
serum sickness
HSN3
52
ITP
HSN2
53
MG
HSN2
54
pemphigus vulgaris
HSN2
55
Rheumatic fever
HSN2
56
type 3 HSN
immune complex deposition which activates complement which attracts neutrophils and these release lysosomal enzymes. Can have vasculitis and systemic manifestations
57
serum sickness
an HSN3 where antibodies to foreign protein are produces and immune complezes deposit and they fix complement
58
arthus reaction
local subacture antibody mediated HSN reaction. INtradermal injection of antigen presented individual leads to complex formation in the skin leading to edema, necrosis, and activation of complement
59
type IV HSN
delayed T cell mediated response when sensitized T cells encounter the antigen then they release cytokines. This leads to macrophage activation.
60
what is the candidal skin test test? what if there is no response to it
HSN4 and have SCID
61
anti-Ach receptor
Myasthenia gravis
62
Anti basement membrane
goodpasture
63
anticadiolipin
SLE
64
anticentromere
CRESt
65
anti-desmoglein
pemphigous vulgaris
66
anti-dsDNA and anti-smith
SLE
67
anti-glutamic acid decarboxylase
type 1 DM
68
antihemidesmosome
bullous pemphigoid
69
antihistone
drug induced lupus
70
anti-jo-1, anti SRP, anti mi-2
polymyositis, and dermatomyositis
71
antimicrosomal, antithyroglobulin
hashimoto
72
antimitochondrial
primary billiary cirrohsis
73
antinuclear
SLE
74
antiparietal cell
pernicious anemia
75
antiphospholipase A2 receptor
primary membranous nephropathy
76
Anti-Scl70 anti DNA toposiomerase
Scleroderma- diffuse
77
antismooth muscle
autoimmune hepatitis
78
anti SSA anti SSB- anti Ro and La
Sjogren syndrome
79
anti TSh receptor
graves disease
80
anti-U1 RNP
mixed CT disorder
81
voltage gated CCB antibodies
Lambert Eaton
82
IgA antiendomyseal and anti tissue transglutaminase
Celiac disease
83
MPO anca/ panca
microscopic polyangiatis, eosinophilic granulomatosis with polyangiitis- Churgg Strauss
84
PR3-anca or cANCA
granulomatosis with polyangiitis-Wegner
85
Rheumatoid factor and anti-CCP
rhematiod arthritis
86
APC
colon cancer
87
BRCA1
breast cancer- DNA repair protein
88
CDKN2A
melanoma and pancreatic cancer- blocks G1- S phase
89
DCC
colon cancer
90
DPC4/SMAD4
pancreatic cancer
91
MEN1
menin- MEN1
92
NF1
RAS gtapse
93
NF2
merlin protein
94
PTEN
breast cancer, prostate cancer, endometrial cancer
95
Rb
retinoblastoma and osteosarcoma- blocks G1 to S phase
96
P53
Li fraumani or otehr cancers- activates p2 and regulates g1 to S and G2 to M
97
TSC1
hamartin protein- tuberous sclerosis
98
TSC2
tuberin protein- tuberous sclerosis
99
VHL
VHL and RCC- inhibits hypoxia inducible factor Ia
100
WT1/WT2
wilms tumor
101
alkaline phsophatase
metastasis to bone or liver- paget of bones
102
alpha fetoprotein
hepatocellular cacrincoma, hepatoblastoma, yolk sac tumor, mized germ cell tumor- high in NT defects
103
CA15-3/Ca27-29
breast cancer
104
CA19-9
pancreatic cancer
105
CA 125
ovarian cancer
106
calcitonin
medullary thyroid carcinoma
107
CEA
increased in pancreatic or colon cancer- produced by gastric, breast, and thyroid
108
PSA
only specific to prostate pathology
109
p-glycoprotein
adrenal cell carcinoma but the cancers that can pump chemo out of the cell
110
cachexia what factors mediate it
mediated by TNF, IFN gamma, and IL1 and 6
111
what mets to the brain
lung, breast, prostate, melanoma, GI
112
what mets to the liver
colon, stomach, pancreas
113
what mets to the bone and is blastic
prostate, testes
114
what mets to the bone and are lytic
rental cell, thyroid
115
what mets to the bone and are blastic and lytic
lung, breast
116
site of synthesis of secretory exported proteins and of N linked oligosaccharide addition to many proteins. It is in the nil bodies to synthesize the peptide NT and free ribosimes are there to synthesize proteins in the sytoplasm. Goblet cells and plasma cells have an increased proportion of this organelle
Rough Er
117
site of steroid synthesis and detox of drugs and poisons. These are in the hepatocytes and steroid hormone producing cells of the adrenal cortex and gonads- which organelle is this
Smooth Er
118
distribution center for proteins and lipids form the ER to the visible and plasma membranes. Ads oligosaccharides and mannose 6 phosphate- what organelle is this
golgi body
119
coarse facial features, cloudy corneas, restricted joints, and high plasma levels of lysosomal enzymes. often have fatal in childhood- what is failing here
there is no mannose 6 phosphate to lysosomal enzymes are secreted instead of directed to the lysosomes
120
COP1 does which direction of transport
golgi to ribosome
121
COPII is which direction of transport
ribosome to golgi
122
what does a peroxisome do
catabolism of very long chain fatty acids, fatty acids, and amino acids and ethanol- it also produces a part of the myelin
123
what does a proteasome do
degrade damaged or ubiquitinated proteins
124
carrier frequency equation
2squareroot(disease prevalence)
125
the frequency of X linked disease in males and females according to hardy weinburg
males=q and females=Qsquared
126
when does hardy weinburg numbers do not work
linkage dis-equalibrim means that these are stuck together which leads differences in the ratio
127
hardy weinburg eqn
psquared+2pq+qsquared: p is homozygois and pQ are heterozygotes
128
effect male and females of each generation
autosomal dominant
129
tend to be more severe disorder and is in only 1 generation overall- if there are two carrier parents then there will be 25% chance of being effected
autosomal recessive
130
more severe in males, and there is a 50% chance of being affected if male- skips generations
X-linked recessive
131
transmitted through either parent- 50% of daughters and sons, fathers transmit to all daughters-
X linked dominant
132
inheritted disorder of increased phosphate wasting at proximal tubules and resultless in rickets- what is it called
hypophosphatemic rickets
133
myopathy, lactic acidosis, CNS disease, stroke like episodes, and failure of oxidative phosphorylation and ragged red fibers
mitochondrial myopathies- transmitted through the mother
134
mutation in FGF3 inhibits chondrocyte prolideration. It presents as dwarfism
achondroplasia
135
what is the enzyme deficient in albinism
tyrosinase
136
intellectual disability, growth retardation, seizures, fair skin, eczema, musty body odor-- what is deficient, what is the treatment, and what aa is bad
due to decreased phenylalanine hydroxylase or tetrahydrobiopterin cofactor- tyrosine is essential because increased phenylalanine is toxic. Treatment is to increase tyrosine in the diet and tetrahydrobiopterin and to decrease PK.
137
what looks different if tetrahydrobiopterin is deficient in PKU
can have increased prolactin and decreased NE. Can have an increased phenylalanine and decreased serotonin.
138
what are the maternal effects of PKU
child will have microcephaly, disability, and heart defects
139
patient has pancreatitis, hepatosplenomegaly, and erupt pruritic xanthomas and a creamy layer of blood- what is the defect, what are the risks associated, and what are the increased blood levels
lipoprotin lipase of ApoC2 def- no increased risk for atheroscelsis- test with hepatic to see LPL activity and body can't clear the dietary lipids- hyperchylomicronemia- AR
140
patient have 700+cholesterol, and accerleared atheroscelosis, tendon xanthomas, and corneal arcus-what is the defect, what are the risks associated, and what are the increased blood levels
familial hypercholesterolemia-AD- increased LDL and cholesterol for missing LDL receptors
141
patient has massive increase in TG which can cause acute pancreatitis-what is the defect, what are the risks associated, and what are the increased blood levels
hyper TG- AD- hepatic overproduction of VLDL
142
steatorrhea and liked red blood cells, ataxia, nightblindness-what is the defect, what are the risks associated, and what are the increased blood levels
decreased APOB48- AR so there is a decreased in apoB100 and a mutation in MTP this leads to decreased VLDL and chylomicrons so increased TAG in enterocytes- cannot get rid of the TAGS- abetalipoproteinmia
143
pharyngitis with pseudomembranes in the throat and sever lymphadenopathy- inactive the elongation factor 2- what is the toxin and disease
diptheria toxin
144
inactives elongation factor EF2- what is the toxin and disease
exotoxin a from pseudomanas
145
inactivates 6- s ribosome from removing adenine from the rRNA- G mucosal damage and dysentary, can cause hemolytic uremic syndrome- what is the toxin and disease
shiga toxin- shigella
146
enhances cytokine release causing HUS and it inactivates the 60S ribosome by removing adenine from rRNA- what is the toxin and disease
Shia like toxin- EHEC O157H7
147
over activates the adenylate cyclase to increase cAMP and increase Cl secretion in the gut and H2O effulx watery diarrhea- what is the toxin and disease- what is the toxin and disease
heat labile LT in ETEC
148
over activation of guanylate cyclase and increase cGMP and decrease responion of Nacl and H2O in the gut. leading to watery diarrhea - what is the toxin and disease
heat stable ETEC
149
mimics the adenylate cyclase enzyme and increased cAMP- edema on the edges on tan eschar- what is the toxin and disease
edema toxin of bacillus anthracis
150
overactivates adenylate cyclase and increase cAMP by permanently activating Gs in the gut and increases the Cl secretion in the gut and water effflux- leas to voluminous rice water stools with increased infection in people with decreased gastric acid- what is the toxin and disease
cholera toxin
151
child coughs on expiration and whoops on inspiration- over activation of adenylate cyclase and this increases cAMP and disables Gi by impairing phagocytosis to permit survival- what is the toxin and disease
pertisus toxin
152
protease that cleaves the SNARE protein and it is required for normal NT release from vesicular fusion- spastic paralysis with rises sardonic and lockjaw and prevents release of inhibitory NT from the Renshaw cells- what is the toxin and disease
tetanospasmin- clostridium tetani
153
protease that cleaves SNARE protein and it is required for NT release from vesicular fusion- flaccid paralysis, floppy babe, toxin prevents release of stimulatory ACH signals from NMJ, can have diplopia, dysphagia, and respiratory depression- what is the toxin and disease
clostridium botulinum-
154
phospholipase that degrades tissue and cell membranes- degradation of phospholipids leading to a double zone of hemolysis on blood agar and myonecrosis- what is the toxin and disease
alpha toxin- perfringins
155
protein that degrades cell membanes- lyses RBC and contributes to beta hemolysis- used to diagnose rheumatic fever streptolysin O- what is the toxin and disease
strep pyogenes- streptolysin O
156
inhibits activation of complement and phagocytosis- what is the toxin and disease
strep pyogenes- protein M
157
binds to MHCII and TCR causing oerwelming release of IL1,IL2,IFNgamma, TNFalpha- shock- fever, rash, and rash
toxic shock syndome in s.aureus and exotoxin A in strep pyogenes
158
which staph is novobiocin resistant
saprophyticus
159
which staph is novobiocin sensitive
epidermidis
160
optochin sensitive
strep pneumo
161
optochin resistant
strep vidians
162
headache, nonproductive cough, patchy or diffuse interstitial infiltrate and X ray looks bad- positive cold agglutination test and can lyse RBC. Not seen on grab stain frequently in young college or military recruits
mycoplasma pneumoniae
163
what does mycoplasma have in its cell wall
sterols for stability
164
what are the CSF findings in bacterial meningitis
increased neutrophils, increased protein, decreased glucose
165
what are the CSF findings in fungal/TB meningitis
increased lymphocytes, increased protein, decreased glucose
166
what are the CSF findings in viral meningitis
increased lymphocytes, normal to increased protein and normal sugar
167
what is the function of alpha1 and what Gprotein are they with
Gq- increased vascular smooth muscle contraction, increased pupillary contraction, increased in intestinal and bladder sphincter muscle tone
168
what is the function of alpha2 and what Gprotein are they with
Gi- decreased sympathetic outflow and decreased insulin release, decreased lipolysis, increased platelet aggregation, decreased aqueous humor production
169
what is the function of beta1 and what Gprotein are they with
Gs- increased heart rate, increased contractility, increased renin release, increased lipolysis
170
what is the function of beta2 and what Gprotein are they with
Gs- vasodilation, bronchodilatiion, increased lipolysis, increased insulin release, decreased uterine tone, cilary muscle relaxation, increased aqueous humor production
171
what is the function of beta3 and what Gprotein are they with
Gs- increased lipolysis, increased thermogenesis in skeletal muscle
172
what is the function of M1 and what Gprotein are they with
Gq- CNS and enteric nervous system- stomach
173
what is the function of M2 and what Gprotein are they with
Gi- decreased heart rate and contractility of the atria
174
what is the function of M3 and what Gprotein are they with
Gq- increased exocrine gland secretion, lacrimal, sweat, salivary, gastric acid, increased gut peristalsis, increased bladder contraction, bronchoconstriction, increased pupil contraction, mitosis and accomidation
175
what is the function of D1 and what Gprotein are they with
Gs- relaxes renal vascular smooth muscle
176
what is the function of D2 and what Gprotein are they with
Gi- modulated tranmitter release in the brain
177
dopamine given at a low dose leads to what
increased heart contraction and increased renal blood flow
178
what is the function of H1 and what Gprotein are they with
Gq- increased nasal and bronchial mucus production, increased vascular permeability, increased contraction of bronchioles, increased parities and pain
179
what is the function of H2 and what Gprotein are they with
Gs- increased gastric acid secretion
180
what is the function of V1 and what Gprotein are they with
Gq- increased vascular smooth muscle contraction like pressers it increases the BP and it increases from constriction
181
what is the function of V2 and what Gprotein are they with
Gs- it increases H2O permeability and reabsorption in collecting tubules of the kidneys
182
what are controlled by Gq
H1, a1, v1, M1, M3
183
what are controlled by Gs
B1, B2, B3, D1, H2,V2
184
what are controlled Gi
M2, a2, D2
185
what connects the tongue to the thyroid in embryonic development- what is the remnant called and what is the embryonic structure called
It is the thyroglossal duct and if it persists it forms the pyramidal lobe of the thyroid
186
where can ectopic thyroid tissue be found and what are the complications if its removed
its called a lingual thyroid and it can lead to hypothyroid if it is the only thyroid tissue present
187
what is a midline neck mass that moves with swallow or protrusion of the tongue
it is a thyroglossal duct cyst
188
what is a lateral neck mass that does not move with swallow
branchial cleft cyst
189
what is the embryonic origin of thyroid tissue and which cells are derived from something different
thyroid is from the endoderm and the parafollicular cells are from neural crest
190
what is the adrenal cortex derived from and what is the adrenal medulla derived from
the cortex is from the mesoderm and the medulla is from the neural crest cells
191
Cushing syndrome- what can cause it
- exogenous steroids- leads to bilateral adrenal atrophy
- primary adrenal adnoma, hyperplasia, or carcinoma- leads to decreased ACTH and increased cortisol- only one large on
- acth pituitary adenoma- increased ACTH so bilateral hypertrophy
192
findings with Cushing
HTN, moon face, striae, tunnel obesity, buffalo hump, osteoporosis, hyperglycemia, amenorrhea, immunosuppression
193
how to diagnose- what is the dexamethasone suppression test
no suppression if its ectopic. Only suppressed if it is from an acth adenoma of the pituitary
194
diabetic ketoacidosis
usually due to insulin noncompliance, increased insulin requirements from stress, excess fat breakdown and increased ketogenesis from increased free fatty acids, which are the name into ketone bodies, Beta hydroxybutarate is increased over acetoacetate. Usually occurs n DM1, as endogenous insulin in DM 2, and prevents lipolysis
195
signs of DKA
delirium, psychosis, Kussmal breathing (deep/rapid breathing), abdominal pain/nausea/vomiting, dehydration, fruity breath odor
196
labs for DKA
hyperglycemia, increased H decreased bicarb, ADMA increased ketones, leukocytosis. hyperkalemia but depleted intracellular K due to transcellualr shift from decreased insulin
197
complications of DKA
mucomycosis or rhizopus, cerebral edma, cardiac arrhythmias, heart failure
198
treat of DKA
IV fluids, insulin, K to replete intracellular stores
199
hyperosmolar hyperglycemia nonkeotic syndrome
state of profound hyperglycemia induced dehydration and increased serum osmolality, seen in elderly with DM 2 with limited ability to drink. Hyperglycemia and excessive osmotic diuresis, dehydration, eventual one of this. Thirst, polyuria, leathery, focal neurological defects, and coma if left untreated
200
labs of hyperosmolar hyperglycemic nonketotic syndrome
increased serum osmolality, hyerpglycemia, no acidosis because the ketone production is inhibited by insulin.
201
treatment of hyperosmolar hyperglycemia nonketotic syndrome
aggressive IV fluids, insulin therapy
202
what are the first treatment strategies of type 1 DM
low carb diet, insulin replacement
203
what are the first treatment strategies of type 2 DM
diet modification, exercise, insulin replacement if lifestyle modification fails
204
which are the rapid acting insulins
lispro, aspart, glulisine- no LAG
205
MOA of insulin
binds the insulin receptor and increases the tyrosine kinase activity quickly. liver increases the glucose stores as glycogen, and increase the glycogen protein synthesis and K uptake, increase TG storage
206
side effects of insulin
hypoglycemia, lipodystrophy, some hypersensitivity reactions
207
short acting insulin
regular insulin
208
intermediate insulin
NPH insulin
209
long acting insulin
detemir, glargine used for basal control of diabetes
210
metformin what does it do
decreased gluconeogenesis, increase glycolysis, increase peripheral glucose uptake, increased insulin sensitivity
211
metformin clincial use
first line with some modest weight loss, can be used in patients with no islet function.
212
metformin risks and ocncerns
GI upset, lactic acidosis in people with renal insufficiency
213
sulfonylureas- names
chloropropamide, tolbutamide, glimepriride, glipizide, glyburide
214
sulfonylureas- MOA
close the K channel in the beta cell which causes the increase release of insulin from depolarization and ca influx.
215
sulfonylurea clinical use
stimulater release of endogenous insulin require some islet cell function.
216
sulfonylureas- risks and concerns
risk of hypoglycemia increased in exercise, missed meals, malnourishment, organ dysfunction, risk is increased in renal failure. there is weight gain. Can have disulfiram reaction, and hypoglycemia
217
glitazones/thiazolidinediones- MOA
increased insulin sensitivity in peripheral tissue bids to PPAR gamma nuclear transcription regulator- it is inranuclear receptor that acts as transcriptional regulator. PPAR is a transcription regulator which decreases the receptors
218
glitazones/thiazolidinediones- clinical use
good for people with renal impairment
219
glitazones/thiazolidinediones- side effects
weight gain, edema, flood retention from increased NA reabsorption in CT. can lead to increase adipose and exacerbation of HF, also hepatotoxic and increased risk of fractures
220
meglitinides- which ones
nateglinide, and repaglinide
221
meglitinides- MOA
stimualte postprandial insulin release by binding to k channels on beta cell membranes
222
meglitinides- clinical use
mono therapy in DM 2 or combined with metformin
223
meglitinides- side effects
hypoglycemia increased risk with renal failure see weight gain
224
GLP1 analogs- which
exantide, liraglutide
225
GLP1 analogs- MOA
increase glucose dependent insulin release, decreased glucagon secretion, decreased gastric emptying, increased satiety
226
GLP1 analogs- side effects
nausea, vomiting, pancreatitis, modest weight loss
227
DDP4 inhibitors- which
gliptins
228
DDP4 inhibitors- MOA
inhibits DPP4 enzyme that activities GLP1 increased glucose dependent insulin release, decrease glucagon release, decreased gastric emptying, increased satiety
229
DDP4 inhibitors- side effects
mild urinary or respiratory infections
230
amylin analogs- which
pramlintide
231
amylin analogs- MOA
decreased gastric emptying, decreased glucagon
232
amylin analogs- side effects
hypoglycemia in the setting of mistimed prandial insulin, and nausea
233
SGLT2 inhibitors- which
flozins
234
SGLT2 inhibitors- MOA
block resorption of glucose at the PCT
235
SGLT2 inhibitors- side effects
avoid with bad kidneys have to look at the Cr and BUN before starting- glucosauria, UTI, vaginal yeast infections, hyperkalemia, dehydration, orthostatic hypotension
236
alpha glucosidase inhibitors- which
acarbose, miglitol
237
alpha glucosidase inhibitors- MOA
inhibit intestinal brush border aha glucosidases. delayed carbohydrate hydrolysis and glucose absorption. decreased postprandial hyperglycemia
238
flip through some abdominal CT
good job
239
what supplies the lower esophagus to proximal duodenum- artery and nerve
celiac artery and vagus nerve
240
what supplies the distal duodenum to proximal 2/3 of the transverse colon- artery and nerve
SMA and vagus
241
what supplies the distal 1/3 of the transverse colon to the upper portion of the rectum- artery and nerve
IMA and pelvic
242
celiac disease
gluten sensitive enteropathy, celiac sprue- autoimmune mediated intolerance of gladian- malabsorption and steatorrhea. Associated with HLA-DQ2 DQ8, northern european descent, dermatitis herpetiformis, decreased bone density. IgA anti-tissue transglutaminase, anti-endomysial, antk-deamindated gliadin peptide antibodies- villous atrophy and crypt hyperplasia with intraepithelial lymphocytosis. increased malignancy- short stature, blasting, diarrhea, and fart, weight loss
243
what is the sudan stain used for
fats are first so this is high confidence of malsoprtion
244
Crohn
skip lesions, rectal sparing, cobblesteone mucosa, creeping fat, bowel wall thickening, noncaseating granluomas and lymphoid aggregates, malabsorption malnutrition, colorectal cancer, increased risk punctilios, abscess/strictures, perianal disease- diarrhea that may or not be bloody. Rash, arteritis, ulcerations. Kidney stones, gallstones- treatment of corticosteroids,
245
what kind of kidney stones does crohns get
calcium oxalate because of decreased calcium oxalate binding
246
treatment of crohns
corticosteroids, azothioprine, antibiotics like ciprofloxacin, metronidazole, infliximab, adailimumab
247
untreated healing crohns has what cytokine present
IL10 which decreases the Th1 activities and the Th1 tends to causes the granulomas
248
ulcrative colitits
ulcers, large intestein, continuous, oclorectal canceer, crypt abscesses, extends proimally, red diarrhea, scelrosis cholangitis. pANCe
249
toxic megacolon symptoms
abdominal pain, fever, air fluid levels, shock, bloody diarrhea, perforation
250
what are the extra intestinal manifestations of inflammatory bowel disease
rash, eye inflammation, oral ulcerations, arthritis
251
treatment of UC
5-aminosalicylac preparations, 6-mercaptopurine, infliximab, colectomy
252
cancer from IBD looks like
younger with flat and non, polyps with signet rings cells early p53 mutations and late APC, proximal colon, multifocal usually 10 years after UC
253
irritable bowel syndrom
recurrnt abdominal pain with pain that improves with defectation, change in stool frequency, change in appearance of stool- middle ages women
254
hemispatial neglect- where is the lesion
nondominant parietal cortex
255
agraphia, aculculia, finger agnosia, left right disorientation- where is the lesion
dominant parietal cortex
256
CN III damage motor output
it is to the ocular muscles- affected primarily by vascular disease and due to decreased diffusion of oxygen and nutrients to the interior firbers from compromised vascular that resides on the outdoes of the nerve. ptosis and down and out gaze
257
what is the parasympathetic output to the CNIII
it is fibers on the peripheray and its first from compression so the sings are diminished or absent pupillary reflex and blown pupil with down and out
258
diabetic CNIII damage-
acute diplopia, down and out from ischemic damage which is at the core then spreads out. The size is normaal-acute has to be down and out first then it can start getting some reactivity
259
compression of CNIII
peripheral is first from the parasympathetic firsts on the outside being compress so there is effect in reactivity to light and its down and out. Typically from posterior communicating and then it can be from uncal herniation
260
CN IV dmage
eyes move upward with contralateral gaze so tilt head towards the eyes of the lesion
261
how can a CN IV lesion present
it can present with compensatory head tilt and trouble going down stairs
262
CN VI palsy
cannot abduct the eye so it cannot move out
263
what is the lesion from if you can only see out of one eye
right anopia- optic nerve lesion
264
what if you can't see the temporal sides of your vision
bitemporal hemianopsia- so have something compressing the optic chiasm like a pituitary adenoma or craniopharyngeoma
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what if you can only see the left parts of your vision
the lesion is at the optic tract and its homonymous hemianopia
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what if you can only see the top quarter of both eyes- pie in the sky
right temporal lesion of MCA- and its from meyers loop
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what if you can only see the bottom quarter of both eyes- pie on the floor
Right pariteal lesion or MCA- its opposite from the side of lesion
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hemianopia with macular sparing
PCA infact
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entral scotoma
only lose the middle of the middle-
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draw the brachial plexus and write out the order of the things
did you actually do it?
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RA pathogenesis
infalmmatory cytokines and cells induce a pannus formation with proliferative fraunaltio information which erodes the cartilage and bone
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RA predisposing facotrs
female, HLDR4, and smoking, and silica exposure.
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what is the more specific test for Ra
it is anti-cyclic citrullinated peptide antibody
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presnsetation of RA
pain, swelling, morning stiffness, lasting under 1 hour. symmetric joint inclement with fever and fatigure
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what test should you get for RA regularly
cervical XR to check for subluxation.
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what joints of the hands does RA not involve
it does not idled the DIP
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what are the treatments for RA
NSAIDs, and methotrexate and sulfasalazine, hydroxychrlorowine, leflunomide, TNF alpha inhibitors
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what can subluxation lead to and what would the symptoms be RA
it is from increased risk of RA and incubation and lead to spinal compression and flaccid paralysis
279
sarcoidosis
widespread noncaseating granulomas- elected ACE, and elevated CD4/CD8- bilateral adenopathy and coarse reticular opacities. Extensive hailer and mediastinal adenopathy. It is associated with restrictive long disease, and erythema podium, lupus perinea on skin, and bell palsy, epithelium granulomas, uveitis, hypercalcemia. increased 1 alpha hydroxylate mediated vitamin D activation.
280
what cytokines are active in sarcoid
it is Th1 and iL2 and IFN gamma increased so macrophages to granulam
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what are the lab levels of calcium and vitamin D for sarcoidoisis
increased 1,5 vitamin D, decreased PTH and increased Ca
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arachadonic acid path
FA 446
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what does airway obstruction lead to in terms of values
decreased FVC, decreased FEV1, decreased ration, and increased TLC
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Chronic bronchitis presentation
it is 3 months over 2 years from smoking large areas. It is glandualr hyperplasia leading to increased mucus which forms plus and then leads to cough and increased PaCO2 and decreased PaO2, and
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chronic bronchitis complications
increased risk of infections and for pulmonate, clamp down to shunt from O2 low region and move it to other areas, but if its all over from disease all over can create increased RH work which led to right heart hypertrophy and failure.
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emphysema presentation
destroy alveolar sacs from exchange so increased collapse because cant have enough elastic roil to stay open. It is dyspnea, airway collapse of small ones, purse lips for increased back pressure to prevent trapping, and pink offer ,weight loss from increased breathing work ,and wide chest from increased chest pull out
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what is emphysema pathophysiology of smoking caused
centracinar emphysema- it is increased proteases because of the extra inflammation which is more than the alpha 1 can handle
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what is the pathophysiology of alpha 1 antitrypsin
it is no protection from protease damage because too much proteases. It is panacean emphysema and lower lobe pneumonia get cirrhosis from misfolded protein build up in the hepatocytes and this causes pink PAS positive globules. these are in the endoplasmic reticulum
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what is the gene for alpha 1 anti-trypsin and what is the difference with a heterozygote and homozygote
-PiM is normal allele and the common mutation is PiZ. If you are homozygous, you will get it. There is PiZ and PiM together then it is you are heterozygous so should not smoke, but need to keep lungs protected because some increased risk from decreased production,
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what are the cytokines that induce asthma
TH2, IL4-IgE, IL5-eosinophils, IL10- inhibit Th1, and so increased Th2
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pathophysiology of asthma
it is re-exposure causes cross linking of IgE and this activates mast cells and dump histamine and causes vasodilation,in venues and it causes fluid from posterior capillary venues. Leukotriene C4, D4,E4- constriction and inflammation leads to bronchoconstriciton and perpetuats the constriction.
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bronchiectaasis
abnormal dilated airways - lose tone and air trapping whorls because the air can't get out. Large airspaces and necrotizing inflammation and damage to the wall
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who gets bronchiectasis
CF (thick sputum), Kartageners (dynein arm less movement), tumor or foreign body, necrotizing infection like Kleb, and allergic bronchopulmonary aspergillum (asthmatics or CF gets HSN reactions to aspergillum.
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what are the complications of bronchiectasis
hypoxia and cor pulmonale, and secondary amyloidosis
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foul smelling sputum, dyspnea, cough
bronchiectasis
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what is the differential for digital clubbing
bronchiextasis, large cell lung cancer, TB, CF, empyema, chronic lung abscess
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what are charcot leyden crystals
they are esonophilic crystals from breakdown of eosinophils in the sputum (bmp)
298
what cell type leads to the emphysema seen in smokers
activation of macrophages of neutrophils and macrophages to damage and increased proteases and decrease antiprotease activity
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what are the benign lung lesions and what can cause them
benign hamartomas and grnulomas (histoplasma and TB)
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what is the bad part of cigarette smoke causing cancer
polycyclic aromatic hydrocarbons
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what do you look for if there is a mass on lesion on the lung
look at old XR to see if anything has changed
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what are hamartomas composed of
calcified on imaging and has cartilage and lung tissue
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small cell lung cancer what does it look like
poor differentiated small cells, central tumor on smokers and increased mitosis
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small cell lung cancer: what are the paraneoplastic syndromes
ADH, ACTH, and Lambert Eaton (presynaptic calcium channels)
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squamous cell carcinoma histology
keratin pearls and intracellular bridges which are desmosomal connections
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where is the squamous cell tumor and what are the paraneoplastic syndromes
PTHrP and increased Ca, and central tumor of male smokers
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large cell tumor histology
poor differentiation with poor prognosis
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bronchioloalveloar tumor
tumor on small airway and malignant Clara cells and peripheral looks like pneumonia and walls of alveoli are replaced by tall columnar cells
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carcinoid tumors
neuroendocrine tumors and polyp mass on the bronchi positive chromogranin
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what cancer is involved or moves to the pleura
adenocarcinoma
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what are some of the complications of lung cancer
pleural involvement (adenocarcinoma), obstruction of the SVC, phrenic or laryngeal nerve, pan coast tumor (pinpoint pupil, and anhidrosis of the forehead , and ptosis
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where does a lung tumor met to
adrenal glands
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what are the things associated with potter sequence or syndrome
pulmonary hypoplasai, oligohydramnios, twisted face, twistedd skin, extremity defects, renal failures in utero
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what are the causes of potter sequence
ARPKD (small cysts on kidneys in utero), obstructive uropathy (prosterior urethral valvees), bilateral renal agenesis, chronic placental insufficiency
315
what poles of the kidneys fuse on horseshoe kidney
it is inferior poles that are fused.
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what does the horseshoe kidney get stuck on
IMA
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what are horseshoe kidneys associated with
hydronephrosis, renal stones, infection, chromosomal aneuploidy and sometimes cancer
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neural crest derivatives
melanocytes, aorticopulmonary septum, ganglia, irirs, chromaffin cells, cranial nerves, odontoblasts, ossibles, parafollicular cells, sclera
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what is the male formation like from the internal and external path
SRY end turns on testis determining factor and it hits the testes and increases the serotli cells
- internal - settle cells secrete mullein inhibitory factor and this degenerates the paramesonephric ducts
- external- the leydig cells are stimulates to secrete testosterone and this cause the wolfing duct to develop which is the internal structures like the everything but the prostate. It then converts to DHT and this is what starts the male external genitalkia
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what happens if there are no sertoli cells or they lack MIF
develop male and female internal genitalia and male external genitalia
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what happens if 5 alpha reductase is deficitnet
inability to convert t to DHT causes male internal genitalia nbut ambigious on the outside- Dominican children that sprout penises at puberty.
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Paramesoneprhic development
no SRY gene, so it develops into female internal structures, fallopian tubes, uterus, upper portion of the vagina
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what happens for mullein agensis
may present as primary amenorrhea due to lack of uterus with females with full functional ovaries and secondary sexual chaaracterisics
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what is the homolog of glans penis
clit
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what is the homolog of crops vavernosu man spongiosum
vestibular bulbs
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what is the homolog of bulbourethral glands
greater vestibular glands
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what is the homolog of prostate gland
urethral and parauterthal glands
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what is the homolog of ventral shaft of the penis
labia minora
329
what is the homolog of scrotum
labia majora
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hypospadia
the opening is on the bottom and its the failure of the urethral folds
331
what other conditions are associated with hypospadias
inguinal hernia, and crytorchidism
332
epispadias
abnoraml opening of the penile urethra on dorsal surface of the penis due to faulty genital tubercle
333
what are the other conditions associated with epispadias
extrophy of the bladder
334
what do the letters of APGAR stand for
```
A-appearance
P- pulse
G-grimace
A-Activity
R-respiration
```
335
what is the APGAR score that requires further evalulation
7 or under
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testicular atrophy, long extremities, gynecomastia, female hair distribution, and intellectual disabiltiy- what in the condition and what are the hormonal level with it
Klinefelter 47 XXY, it is increased LH and Increased FSH and decreased T and since there is dysgenesis of the seminiferous tubules that is why the FSH is high and the bas normal leydig cells decrease the T and increase the LH and estrogen from the extra androgens hanging around
337
female with short stature, ovary dysgenesis, shield chest webbed neck, cystic hydra, llynpahedam of hands and feet- what in the condition and what are the hormonal level with it
it is a Turner syndrome 45XO- there is decreased estrogeen which leads to increased LH and FSH. Some are mosaic which is somatic mosaicism. it is the most common form of primary ammenorhea
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what are the conditions associated with Turner syndrom
bicuspid aortic valve, horseshoe kidney, and coarction of the aorta
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is pregnancy possible with Turner
yes if you give them IVF, exogenous estradiol 17b and progesterone
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what are double Y males like
phenotypically normal but very tall may be assocaited wit severe acne, learning disability, autism spectrum
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ovotesticular disorder of sexual development
both ovarian and testicualr tissue is present wit ambiguous genitalia- true hermaphroditism
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PCOS- hormones and what happesn
hyperinsulinemia and or insulin resistance hypothesized to alter the hypothalamic hormonal feedback response and so this increases LH and FSH and increased androgens like testosterone from the theca cells and this decreases the rate of follicular maturation and leads to unruptured follicles and involution
343
what is the presentation of PCOS
it is bilateral large cystic ovaries wit amenorrhea, oligomenrrhea, hirsutism, acnes, and decreased fertility associated with obesitiy
344
what cancer is associated with PCOS
endometrial cancer from the opposed estrogen of anovulatory cycels
345
how do you treat PCOS
OCPS, weight reduction, clomiphene, ketoconazole, spirolactone
