ETP- reproductive quiz Flashcards
(124 cards)
1
Q
According to the diagnostic guidelines, which patient should be referred for further evaluation with respect to fertility?
Question 1 Answer
a.
a 39 year old woman who has been trying to conceive for 3 months
b.
a 35 year old woman who has been trying to conceive for 9 months
c.
a 27 year old woman who has had a miscarriage
d.
a 30 year old woman who has been trying to conceive for 6 months
A
b.
a 35 year old woman who has been trying to conceive for 9 months
2
Q
All of the following are actions of oxytocin on the associates structures except?
Question 2 Answer
a.
milk production in the mammary glands
b.
vasodilation of the vasculature
c.
smooth muscle contraction in the uterus
d.
reduced release of ACTH and TSH from anterior pituitary
A
a.
milk production in the mammary glands
prolactin is for milk production, oxytocin is for milk ejection
3
Q
Considering the production of sperm, the __________ cells produce mature sperm that are secreted into the lumen of the ________________ .
Question 3 Answer
a.
Sertoli; seminiferous tubules
b.
Leydig; seminiferous tubules
c.
Sertoli; rete testis
d.
Leydig; rete testis
A
a.
Sertoli; seminiferous tubules
4
Q
Of the 4 types of prostatitis, which type is most common and which type is most easily treated with antibiotics?
Question 4 Answer
a.
Type III is most common and Type I is most easily treated with antibiotics
b.
Type I is most common and Type III is most easily treated with antibiotics
c.
Type I is most common and Type I is most easily treated with antibiotics
d.
Type III is most common and Type III is most easily treated with antibiotics
A
a.
Type III is most common and Type I is most easily treated with antibiotics
5
Q
types of prostatitis
A
Type I – Acute Bacterial
Cause: Bacteria (E. coli)
Onset: Sudden
Symptoms: Fever, dysuria, perineal pain
Diagnosis: Positive urine culture
Treatment: Antibiotics
Type II – Chronic Bacterial
Cause: Recurrent bacteria
Symptoms: Recurrent UTIs, pelvic pain
Diagnosis: Bacteria in prostate secretions
Treatment: Long-course antibiotics
Type III – Chronic Pelvic Pain Syndrome (CPPS)
Most common type
Cause: Nonbacterial
Subtypes: IIIA (inflammatory), IIIB (non-inflammatory)
Symptoms: Pelvic pain >3 months
Treatment: Alpha-blockers, NSAIDs, multimodal
Type IV – Asymptomatic Inflammatory
No symptoms
Found incidentally
Diagnosis: WBCs in semen/prostate fluid
Treatment: None needed
6
Q
The cellular levels of 5-alpha reductase enzymes would presumably be high in all of the following tissues except?
Question 5 Answer
a.
prostate
b.
skeletal muscle
c.
skin
d.
adipose
A
d.
skeletal muscle
Skeletal muscle mainly responds to testosterone, not DHT.
5 alpha reductase is to convert testosterone into DHT
7
Q
What cell type are most testicular cancers derived from?
Question 6 Answer
a.
germ cells
b.
interstitial cells
c.
stromal cells
d.
granulosa cells
A
a.
germ cells
8
Q
What is the most common position of the uterus?
Question 7 Answer
a.
anteflexed, anteverted
b.
anteflexed, retroverted
c.
retroflexed, retroverted
d.
prolapsed
A
a.
anteflexed, anteverted
9
Q
What is the most common symptom associated with an endometrial carcinoma?
Question 8 Answer
a.
infertility
b.
dysmenorrhea
c.
dyspareunia
d.
bloody vaginal discharge
A
d.
bloody vaginal discharge
10
Q
Which hormone is secreted in large amounts by the corpus luteum?
Question 9 Answer
a.
hCG
b.
Estriol
c.
Progesterone
d.
Estradiol
A
c.
Progesterone
11
Q
Which of the following physiological features are decreased during pregnancy?
Question 10 Answer
a.
tidal volume
b.
stroke volume
c.
residual volume
d.
insulin resistance
A
c.
residual volume
Because lung space is reduced by the enlarging uterus,
12
Q
Which of the following statements with respect to ovarian cancers is true?
Question 11 Answer
a.
ovarian germ cells can give rise to choriocarcinomas and are the most common source of ovarian cancers
b.
stromal cells give rise to ovarian cancers most commonly and ovarian cancers arising from germ cells have the worst prognoses
c.
ovarian cancer with the worst prognosis come from surface epithelial cells that can give rise to serous adenocarcinomas
d.
teratomas are made up of several cell lineages and arise from granulosa cells
A
ovarian cancer with the worst prognosis come from surface epithelial cells that can give rise to serous adenocarcinomas
13
Q
Which of the following statements with respect to pregnancy and lactation is false?
Question 12 Answer
a.
suppression of GnRH via increased prolactin often causes breastfeeding women to be amenorrheic
b.
relaxin reduces premature labour early in pregnancy, but can induce labour later in pregnancy
c.
the placenta produces progesterone and hPL and is delivered in the second stage of labour
d.
oxytocin increases production of prostaglandins which are responsible for cervical ripening and dilation
A
c.
the placenta produces progesterone and hPL and is delivered in the second stage of labour
14
Q
Which of the following with respect to male germ cells is true?
Question 13 Answer
a.
spermatogonium are the least mature and are diploid
b.
primary spermatocytes are the least mature and are diploid
c.
sperm cells are the most mature and are diploid
d.
spermatids are the most mature and are haploid
A
a.
spermatogonium are the least mature and are diploid
15
Q
Which set of symptoms and/or lab findings listed below would be most indicative of a patient experiencing eclampsia?
Question 14 Answer
a.
headache, edema, shortness of breath
b.
edema, proteinuria, high blood pressure
c.
hemolysis, low platelets, elevated liver enzymes
d.
high blood pressure, convulsion, headache
A
d.
high blood pressure, convulsion, headache
16
Q
pre eclampsia
A
Pre-eclampsia
Definition: New-onset hypertension (≥140/90 mmHg) after 20 weeks gestation + proteinuria
OR signs of end-organ damage (even without proteinuria)
Proteinuria: ≥300 mg/24hr or protein/creatinine ratio ≥0.3
Other findings: Edema, headache, visual changes, elevated liver enzymes, low platelets
17
Q
eclampsia
A
Definition: Pre-eclampsia + seizures (not explained by another cause)
18
Q
pre eclampsia vs eclampsia
A
high BP (>140/90) after 20 weeks pregnancy plus proteinuria (or end organ damage)
in eclampsia it is also that but plus seizures
19
Q
With respect to female reproductive cycles, which statement is true?
Question 15 Answer
a.
the proliferative phase refers to development of the follicle and features increasing levels of estrogen
b.
the follicular phase features low levels of progesterone and precedes ovulation
c.
the secretory phase features high levels of progesterone and refers to ovulation
d.
the luteal phase occurs concurrently with the menstrual phase and features low levels of estrogen
A
b.
the follicular phase features low levels of progesterone and precedes ovulation
20
Q
opoid receptors function
A
reduce pain, sedation, decrease respiratory function and GI motility, nausea, miosis, suppress cause, induce euphoria, decrease depression
21
Q
which opioid has highest affinity for mu opioid receptor
A
endomorphins
22
Q
which opioid inhibits GABA and disinhibits dopamines; causing euphoria and where are they found
A
endorphins; in pituitary and hypothalamus
23
Q
most common neurotransmitter of the body and its impacts
A
glutamate; excitatory
24
Q
synthesis of GABA
A
from glutamate (excitatory) into GABA (inhibitory) via L-glutamic acid decarboxylase (a pyridoxine dependent enzyme)
25
where is GABA most in the brain
basal ganglia, hypothalamus, and periaqueductal grey
26
GABA activity is terminated by
uptake into astrocyte glia
27
glycine
excitatory or inhibitory? receptor?
in spinal cord and brain stem; inhibitory
its receptor is chloride channel
28
cerebral infarction (ischemic stroke)
occlusion of arteries serving brain causing hypoxia or anoxia
via thrombosis (from atherosclerosis) or embolism
most common site is middle cerebral artery --> contralateral paralysis, motor and sensory defects and aphasia
29
encephalopathy
global brain dysfunction → altered mental status (acute or chronic)
⚠️ Key Clinical Features:
Altered mental status (confusion, disorientation)
Memory impairment
Personality changes
Sleep disturbances
Seizures (sometimes)
Coma (in severe cases)
i.e. could be hepatic, hypertensive, infectious, traumatic etc
30
intracranial hemorrhage
bleeding onto brain surface
subarachnoid hematoma: rupture of aneurysm --> neurological deficits, headaches, unilateral eye pain
subdural hematoma: low pressure venous blood gets pushed into space between arachnoid and dura and then clots
epidural hematoma: from skull fracture, blunt trauma, usually from arteries
31
most common cause of intracranial hemorrhage
what area most effected and sx
hypertension
most often in basal ganglia causing motor problems like ataxia and chorea
32
alzheimers disease
most important cause of dementia
causes: decreased acetylcholine production or abnormal amyloid gene expression
characterized by: neuritic plaques, neurofibrillary tangles, and grnaulovascular degeneration and atrophy of cerebral cortex
neurofibrillary tangles of tau proteins
beta amyloid
risks: apolipoprotein Ee-4
33
risk for alzheimers
apolipoprotein Ee-4
34
characteristics of alzheimers
Amyloid plaques: Extracellular deposits of β-amyloid peptide
Neurofibrillary tangles (NFTs): Intracellular aggregates of hyperphosphorylated tau protein
Neuronal loss: Especially in the hippocampus and cerebral cortex
Cortical atrophy: Shrinkage of brain tissue, most notably in the temporal and parietal lobes
35
sx of alzheimers
Progressive memory loss: Especially recent (short-term) memory
Impaired language and visuospatial skills
Executive dysfunction: Difficulty planning, organizing, and problem-solving
Behavioral changes: Mood swings, agitation, apathy
Late stages: Loss of motor skills, incontinence, and mutism
36
amyotrophic lateral sclerosis (ALS)
causes? sx?
lower and upper motor neuron disease + atrophy of skeletal muscles
assocaited with mutations in Cu,Zn-superoxide dismutase and glutamate transporter abnormalities
sx: symmetric atrophy and fasciculation (contraction or twitching), exaggerated DTR, spasticity
37
spinocerebellar degeneration
several diseases: extrapyramidal breakdown of spinocerebellar tracts with resultant primary symptom of ataxia
most common is Friedrich's ataxia, autosomal recessive
--> multi limb ataxia, skeletal malformations, mental retardation
38
huntington's chorea
autosomal dominant, extrapyramidal disease; atrophy or basal ganglia (caudate nucleus and putamen) and frontal Cortex
sx: athetoid (slow, writhing, involuntary) movements and progress with deterioration to hypertonicity, incontinence, anorexia, weight loss, dementia
39
huntingtons
1. Genetics
Autosomal dominant neurodegenerative disorder
Caused by CAG trinucleotide repeat expansion in the HTT gene on chromosome 4
More repeats → earlier onset (anticipation)
2. Pathology
Degeneration of the caudate nucleus and putamen (striatum)
Loss of GABAergic medium spiny neurons
Leads to imbalance in basal ganglia circuits → movement disorders
sx: chorea (involuntary dance movement), dystonia and rigidity, dementia, depression and anxiety
40
genetics for huntingtons
Autosomal dominant neurodegenerative disorder
Caused by CAG trinucleotide repeat expansion in the HTT gene on chromosome 4
41
brain region impacted in huntingtosn
Degeneration of the caudate nucleus and putamen (striatum)
42
brain region in parkinsons
dopaminergic neurons in the substantia nigra pars compacta, leading to dopamine deficiency in the basal ganglia.
43
sx in parksinsons
Tremor:
Resting tremor, often described as a “pill-rolling” tremor of the hands; typically asymmetric and occurs at rest, disappearing with voluntary movement.
Rigidity:
Increased muscle tone causing stiffness; can be “cogwheel” rigidity (ratchet-like resistance during passive movement).
Akinesia (or bradykinesia):
Slowness or poverty of movement; difficulty initiating and executing movements.
Postural instability:
Impaired balance and coordination leading to frequent falls, especially in later stages.
Other clinical signs:
Shuffling gait with decreased arm swing
Masked facies (reduced facial expression)
Micrographia (small handwriting)
Hypophonia (soft speech)
Stooped posture
Autonomic symptoms: constipation, orthostatic hypotension, sweating abnormalities
Cognitive decline and dementia can occur in advanced stages
44
parkinsons
Cause: Loss of dopamine neurons in substantia nigra → basal ganglia dysfunction
Classic motor signs: Tremor, rigidity, akinesia/bradykinesia, postural instability
Non-motor symptoms: Autonomic dysfunction, cognitive decline, mood disorders
45
Gillian barre syndrome
autoimmune-mediated demyelinating polyneuropathy causing rapid-onset muscle weakness and sometimes paralysis.
2. Etiology:
Often follows an infection (commonly Campylobacter jejuni, also CMV, EBV, Mycoplasma) by 1-3 weeks
Autoimmune attack on peripheral nerve myelin or axons
3. Pathophysiology:
Immune system attacks the myelin sheath (most common variant) or sometimes axons
Leads to slowed nerve conduction and muscle weakness
4. Clinical Features:
Symmetrical ascending muscle weakness starting in the legs and moving upward
Areflexia (loss of deep tendon reflexes)
Paresthesias (tingling or numbness)
Possible cranial nerve involvement (facial weakness, bulbar symptoms)
Autonomic dysfunction (tachycardia, blood pressure fluctuations)
Respiratory muscle weakness → risk of respiratory failure
46
Gillian barre
Definition: Acute autoimmune demyelinating polyneuropathy causing rapid, ascending muscle weakness.
Cause: Usually triggered by infections (e.g., Campylobacter jejuni), leading to immune attack on peripheral nerve myelin.
Clinical Features: Symmetrical ASCENDING weakness starting in legs, areflexia, possible sensory changes, cranial nerve involvement, and autonomic dysfunction; risk of respiratory failure.
47
most common demyelinating disease
multiple sclerosis (MS)
48
multiple sclerosis (MS)
1. Definition:
Chronic, immune-mediated demyelinating disease of the central nervous system (CNS)
Characterized by inflammation, demyelination, and axonal damage
2. Pathophysiology:
Autoimmune attack on myelin sheaths of CNS neurons
Results in plaque formation in white matter of brain and spinal cord
Disrupts nerve conduction → neurological symptoms
Common signs:
Optic neuritis (painful vision loss)
Internuclear ophthalmoplegia (impaired horizontal eye movement)
Sensory disturbances (numbness, paresthesias)
Weakness and spasticity
Ataxia and gait instability
Bladder dysfunction
usually in women 20-40yrs
Relapsing-remitting or progressive
49
perivenous encephalomyelitis
It is an immune-mediated inflammatory demyelinating disease of the CNS, typically monophasic, occurring after 7-14 days after infection or vaccination
sx:
Fever, headache, lethargy
Seizures
Ataxia, weakness
Optic neuritis
Sometimes coma
50
cerebral edema
accumulation of excess fluid in the brain parenchyma, leading to increased intracranial pressure (ICP) and potentially herniation or brain damage.
Clinical Features:
Headache
Nausea, vomiting
Altered mental status
Papilledema (on fundoscopy)
Seizures
Coma or herniation (in severe cases)
51
types of cerebral edema
Vasogenic edema
🔸 Cause: Breakdown of the blood-brain barrier
🔸 Fluid leaks from vessels into extracellular space
🔸 Common in: Tumors, abscesses, trauma, inflammation
🔸 Most common type
Cytotoxic edema
🔸 Cause: Cellular injury → Na⁺/K⁺ pump failure → intracellular swelling
🔸 Common in: Ischemia, hypoxia, early stroke
🔸 Fluid shifts into cells
Interstitial edema
🔸 Cause: Obstructive hydrocephalus → CSF buildup around ventricles
🔸 Fluid moves from CSF into surrounding white matter
Osmotic edema
🔸 Cause: Hypoosmolar states (e.g., rapid hyponatremia correction)
🔸 Water moves into brain cells
52
hydrocephalus
abnormal accumulation of cerebrospinal fluid (CSF) within the ventricular system of the brain, leading to ventricular dilation and often increased intracranial pressure (ICP).
53
communicating vs non-communicating hydrocephalus
Communicating Hydrocephalus
Cause: Impaired CSF absorption (e.g., arachnoid granulations)
CSF flow is intact, but not reabsorbed properly
Common causes: Meningitis, subarachnoid hemorrhage, post-infectious scarring
Non-communicating (Obstructive) Hydrocephalus
Cause: Physical blockage of CSF flow within ventricles
Examples: Aqueductal stenosis, tumors, cysts
Ventricles upstream of blockage enlarge
54
hepatic encephalopathy
a reversible neuropsychiatric syndrome caused by liver dysfunction, where toxins (especially ammonia) accumulate and impair brain function.
sx:
-flapping tremor
Mental status changes (ranging from confusion → stupor → coma)
Disorientation, irritability, lethargy
Asterixis ("flapping tremor")
Slurred speech
Sleep-wake reversal
Fetor hepaticus (musty odor to breath)
55
peripheral neuropathy
Peripheral neuropathy is damage or dysfunction of peripheral nerves (motor, sensory, or autonomic), leading to weakness, numbness, pain, or autonomic symptoms, usually in a stocking-glove distribution.
🔹 Causes (DANG THE RAPIST mnemonic):
| D | Diabetes mellitus (most common in North America) |
| A | Alcoholism (nutritional deficiency — B1, B12) |
| N | Nutritional deficiencies (B1, B6, B12, E) |
| G | Guillain-Barré Syndrome |
| T | Toxins (e.g. chemotherapy, heavy metals, isoniazid) |
| H | Hereditary (Charcot-Marie-Tooth) |
| E | Endocrine (hypothyroidism) |
| R | Renal failure (uremic neuropathy) |
| A | Amyloidosis |
| P | Paraneoplastic syndromes |
| I | Infections (HIV, Lyme, leprosy) |
| S | Sarcoidosis |
| T | Trauma or compression (carpal tunnel, sciatica) |
🔹 Types:
Sensory neuropathy: Numbness, tingling, burning, pain
Motor neuropathy: Weakness, muscle wasting, fasciculations
Autonomic neuropathy: Orthostatic hypotension, gastroparesis, anhidrosis
56
vitmain b12 deficiency effects
pernicious anemia (megalobaslatic) and neuropathy from demyelination of CNS neurons
57
wernicke Korsakoff from what deficiency
Thiamine (Vitamin B1) deficiency
Common in alcoholism, malnutrition, or malabsorption (e.g., bariatric surgery, chronic vomiting)
58
symptoms of wenicke korsakoff
🔹 Wernicke Encephalopathy (Acute phase)
🔸 Classic triad:
1. Confusion (encephalopathy)
2. Ophthalmoplegia (e.g., nystagmus, lateral rectus palsy)
3. Ataxia (broad-based gait)
Medical emergency — reversible if treated quickly
Lesions in mammillary bodies, thalamus, periaqueductal gray
🔹 Korsakoff Syndrome (Chronic phase)
🔸 Persistent memory impairment, especially:
Anterograde amnesia (can't form new memories)
Retrograde amnesia
Confabulation (making up stories to fill memory gaps)
Lack of insight into deficits
Often follows untreated Wernicke's encephalopathy
Damage mainly in mammillary bodies and medial thalamus
59
trisomy 21/ aka down syndrome
third copy of chromosome 21
60
leukodystrophies
group of diseases characterized by abnormal development or destruction of white matter (myelin) in the central nervous system (CNS).
They involve defective synthesis or maintenance of myelin, leading to progressive neurological deterioration, especially in children.
sx:
Progressive motor and cognitive decline
Hypotonia → spasticity
Ataxia
Seizures
Developmental regression
Vision and hearing loss (in some forms)
61
phenylketonuria (PKU)
PKU is an autosomal recessive metabolic disorder caused by a deficiency of the enzyme phenylalanine hydroxylase (PAH), which converts phenylalanine → tyrosine.
🔹 Cause:
Phenylalanine hydroxylase deficiency → accumulation of phenylalanine
Excess phenylalanine is toxic to the developing brain
Leads to intellectual disability, developmental delays, and neurologic damage if untreated
Affects melanin production (since tyrosine is a precursor)
sx:
Normal at birth (symptoms appear as phenylalanine builds up)
Intellectual disability (preventable with early treatment)
Seizures
Microcephaly
Musty/mousy body odor (due to phenylacetate)
Hypopigmentation (fair skin, hair, blue eyes)
Eczema
**MUST restrict phenylalanine in diet
62
phenylketonuria - what enzyme is deficient
phenylalanine hydroxylase
which turns phenylalanine --> tyrosine
63
hurlers disease
rare, autosomal recessive lysosomal storage disorder caused by a deficiency of the enzyme α-L-iduronidase, leading to accumulation of glycosaminoglycans (GAGs) (specifically heparan sulfate and dermatan sulfate).
sx:
Coarse facial features (gargoyle-like facies)
Developmental delay → progressive intellectual disability
Hepatosplenomegaly
Corneal clouding (a distinguishing feature from some other MPS types)
Dysostosis multiplex (skeletal abnormalities seen on X-ray)
Short stature
Hearing loss
Frequent respiratory infections
Cardiomyopathy or valvular heart disease
Joint stiffness, claw hand deformity
64
Wilsons disease - what is deficient/ what mineral is causing the problem?
autosomal recessive disorder of copper metabolism, causing toxic accumulation of copper in tissues, especially the liver, brain, and cornea.
🔹 Cause:
Mutation in the ATP7B gene → defective copper transport and excretion into bile
Copper accumulates in hepatocytes → spills into bloodstream → deposits in other organs
sx:
Hepatic: Chronic hepatitis, cirrhosis, fulminant liver failure
Neurologic: Tremor, dysarthria, dystonia, Parkinsonism, chorea, ataxia
Psychiatric: Personality changes, depression, psychosis
Ophthalmologic: **Kayser-Fleischer rings** (copper deposits in Descemet’s membrane of cornea)
Other: Hemolytic anemia, renal tubular dysfunction
65
key findings in Wilson disease from the copper buildup
Hepatic: Chronic hepatitis, cirrhosis, fulminant liver failure
Neurologic: Tremor, dysarthria, dystonia, Parkinsonism, chorea, ataxia
Psychiatric: Personality changes, depression, psychosis
Ophthalmologic: **Kayser-Fleischer rings** (copper deposits in Descemet’s membrane of cornea)
Other: Hemolytic anemia, renal tubular dysfunction
66
medulloblastoma
highly malignant, embryonal tumor of the cerebellum, classified as a primitive neuroectodermal tumor (PNET), primarily affecting children.
🔹 Clinical Features:
Signs of increased intracranial pressure: headache, nausea, vomiting
Ataxia and truncal instability (due to cerebellar involvement)
Possible nystagmus, dysmetria
🔹 Pathology:
Highly cellular tumor with small round blue cells
Homer Wright rosettes may be present
High mitotic index and rapid growth
67
meningiomas
typically benign, slow-growing tumors that arise from the arachnoid cap cells of the meninges (the protective layers surrounding the brain and spinal cord).
Symptoms result from mass effect or compression of adjacent brain structures
Headache, seizures
Focal neurological deficits depending on tumor location
Occasionally incidental finding (asymptomatic)
68
neuroblastoma
malignant tumor of neural crest origin arising from the sympathetic nervous system, most commonly from the adrenal medulla or paraspinal sympathetic ganglia.
🔹 Clinical Features:
Abdominal mass (often large, may cross midline)
Horner’s syndrome (if cervical sympathetic chain involved)
Opsoclonus-myoclonus syndrome (paraneoplastic)
Systemic symptoms: Fever, weight loss
Bone pain if metastasized
🔹 Pathology:
Small, round, blue cell tumor
Homer Wright rosettes may be seen
Tumor produces catecholamines (VMA and HVA metabolites elevated in urine)
69
neuroblastoma- what does the tumor produce and what would be in urine
produces catecholamines; VMA and HVA metabolites are elevated in urine
70
neuroglia tumors (astrocytomas and oligodendrogliomas)
Astrocytomas come from astrocytes and range from benign (pilocytic) to very aggressive (glioblastoma). They occur mainly in cerebral hemispheres and cause headaches, seizures, and neurological symptoms. Treatment includes surgery, radiation, and chemo; prognosis varies by grade.
Oligodendrogliomas arise from oligodendrocytes, usually in adult frontal lobes. They often present with seizures, show calcifications on imaging, and have a better prognosis due to 1p/19q co-deletion. Treatment is surgery plus radiation and chemotherapy.
71
oligondendromas
Cells have a classic "fried-egg" appearance under microscope.
Typical "chicken-wire" capillary pattern.
72
neuronal tumors
Neuronal tumors are rare, often benign brain tumors from neurons, commonly causing seizures. Surgical removal usually leads to good outcomes.
73
schwannoma
benign tumors arising from Schwann cells, which form the myelin sheath around peripheral nerves.
Schwannomas are benign nerve sheath tumors, often affecting the vestibulocochlear nerve (ACOUSTIC NERUOMA) and causing hearing and balance issues. Diagnosis is by MRI, and treatment is surgical or radiosurgical.
74
neurofibromatosis
NF1(von Recklinghausen Disease) involves neurofibromas and café-au-lait spots with skeletal and CNS involvement.
(NF1 is a tumor suppressor gene on chromosome 17)
NF2 is characterized by bilateral vestibular schwannomas and multiple CNS tumors.
(NF2 on chromosome 22)
Both are inherited tumor suppressor gene disorders requiring monitoring and symptomatic care.
75
acoustic neruoma
CN VIII;
Unilateral sensorineural hearing loss (most common initial symptom)
Tinnitus (ringing in the ear)
Balance problems / dizziness
type of schwannoma
76
arboviruses
via mosquitos
ssRNA viruses
77
botulism
honey for infant botulism
clostridium botulism has 7 neurotoxins
i.e. food borne outbreaks
toxin from gut carried by blood to peripheral nerves; can block Ach release and cause flaccid paralysis. protease to chew up proteins
sx: N/V, ab cramp, diarrhea, urinary retention, flaccid paralysis beginning with ocular muscles into respiratory muscles (failure)
78
brain abscess
infections: stap and strep usually
can speead from sinuses, eyes, ears, teeth etc
Brain abscess is a focal brain infection causing a pus-filled cavity, presenting with headache, fever, and neurological signs. Diagnosis is by imaging, and treatment requires antibiotics and often surgical drainage.
79
fungal infections
rare; usually if immune compromised (diabetes, AIDS, cancer etc
80
dx of herpes virus
cell culture; ELISA, or PCR on lesion
81
varicella zoster
chicken pox --> shingles
DNA enveloped herpes virus
82
where does varicella zoster virus lay latent in
dorsal root ganglia
83
Epstein barr virus "kissing disease"
EBV is a double-stranded DNA virus, enveloped, belonging to the Herpesviridae family (specifically gammaherpesvirus).
It establishes latent infection primarily in B lymphocytes.
🔹 Cell Tropism and Pathogenesis:
Infects B cells via CD21 receptor and epithelial cells of the oropharynx.
Causes B cell proliferation and immortalization.
Can also infect some T and NK cells indirectly, but B cells are the primary reservoir.
During acute infection, IgM antibodies to viral capsid antigen (VCA) appear first.
IgG antibodies to VCA develop later and persist lifelong, indicating past infection.
🔹 Clinical Manifestations:
Infectious mononucleosis (IM):
Fever, sore throat, tonsillar exudates
Posterior cervical lymphadenopathy
Splenomegaly
Fatigue
Hepatitis (mild transaminitis)
Other associations:
Burkitt lymphoma (especially endemic African type)
Hodgkin lymphoma
Nasopharyngeal carcinoma
Oral hairy leukoplakia (in immunocompromised)
Post-transplant lymphoproliferative disorder (PTLD)
84
dx of Epstein bar
Diagnosis involves heterophile antibody test, EBV serologies (IgM, IgG), and blood smear showing atypical lymphocytes.
85
cytomegalovirus (CMV)
DNAenveloped herpes virus
It establishes latent infection mainly in monocytes/macrophages and various tissues.
🔹 Transmission:
Spread via body fluids: saliva, urine, blood, breast milk, sexual contact, and organ transplantation.
🔹 Pathogenesis:
Infects a wide range of cells, especially epithelial cells, endothelial cells, and monocytes.
Causes cytomegaly with characteristic “owl’s eye” intranuclear inclusion bodies.
🔹 Clinical Manifestations:
Usually asymptomatic in immunocompetent individuals or causes a mild mononucleosis-like syndrome (fever, fatigue, lymphadenopathy) without heterophile antibodies.
Congenital CMV infection: leading cause of non-hereditary sensorineural hearing loss, microcephaly, petechiae, and “blueberry muffin” rash.
Immunocompromised patients: Severe disease including retinitis (leading to blindness), esophagitis, colitis, pneumonitis, and encephalitis.
86
how is cytomegalovirus (CMV) recognized by
multinucleate giant cells with intranuclear inclusions
87
human herpes virus 6 (HHV6)
roseola infantum/ slapped cheeks
Sudden high fever for 3–5 days, followed by a rose-pink maculopapular rash as fever resolves
Febrile seizures may occur during the febrile phase.
infects CD4+ cells
88
HHV6
HHV-6 is a beta-herpesvirus causing roseola infantum in young children, characterized by high fever and a sudden rash. It infects CD4+ T cells and can reactivate in immunocompromised patients, with diagnosis mainly clinical and treatment supportive.
89
leprosy
mycobacterium leprae
infects macrophages and Schwann cells in peripheral nerves.
Causes nerve damage leading to loss of sensation and muscle weakness.
Leprosy is a chronic mycobacterial infection affecting skin and peripheral nerves. Tuberculoid type shows strong immunity with few lesions; lepromatous type shows weak immunity with widespread lesions and high bacterial load. Diagnosis is by biopsy and acid-fast stain; treated with multidrug therapy.
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mycobacteria are
acid fast
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meningitis
E coli (main cause in newborns bc IgM cant pass placental barrier), h influenza b, strep pneumonia (main cause in adults), neisseria meningitides
sx: headaches, vomit, fever
**cervical rigidity especially in infants
Classic triad:
Fever
Nuchal rigidity (neck stiffness)
Altered mental status
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poliomyelitis
poliovirus (ssNRA< no enveleope)
In some cases, it crosses the blood-brain barrier and infects the anterior horn cells of the spinal cord, leading to destruction of lower motor neurons.
sx: fever, fatigue, headache, vomit, stiff neck but can lead to flaccid asymmetric paralysis of the legs
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prion disease
Prion diseases (also called transmissible spongiform encephalopathies) are a group of rare, fatal neurodegenerative disorders caused by abnormally folded proteins called prions.
non viral glycoproteins
spread via eating infected tissue, ogrgan trransplants or iatrogenic
for example creutzefled Jacob disease (mad cow) = dementia, myoclonus, ataxia
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progressive multifocal leukoencephalopathy
PML is a fatal demyelinating disease of the central nervous system caused by reactivation of JC virus (John cunningham) in immunocompromised individuals.
infects astrocytes and oligodendrocytes --> demyelinate
neurological, hemiparesis, ataxia, motor problems
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subacute sclerosis panencephalitis
rare, progressive, and fatal neurodegenerative disease caused by a persistent mutated measles virus infection in the central nervous system.
effects grey and white matter
Clinical Course:
Progresses through stages over months to years:
Behavioral and cognitive decline: personality changes, poor school performance
Myoclonus: sudden, involuntary jerks
Progressive neurologic deterioration: spasticity, ataxia, vision loss
Decerebrate rigidity, coma, and eventually death
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tetanus
clostridium tetani (gram positive rod)
get into contaminated wounds
makes tetanospasmin (neurotroxin) to block inhibitory neurotransmitters like GABA and glycine --> disinhibited motor activity
Clinical Features:
Incubation: ~3–21 days after injury
Trismus (lockjaw) – early sign
Risus sardonicus – grimace-like facial spasm
Opisthotonos – arching of back due to paraspinal muscle contraction
Painful, sustained muscle spasms
May involve respiratory muscles → respiratory failure
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contusion
focal bruising of the brain (blunt trauma)
Capillary rupture → bleeding into brain parenchyma
focal neurological signs
hemorrhage on CT/MRI
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concussion
transient loss of awareness of memory then can have longer term dizziness, depression, apathy, headache
from blunt roam
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carpal tunnel syndrome
median nerve trapped in carpal retinaculum
wrist and hand weakness, radiating pain into lateral palmar and median dorsal side
risks: pregnant, repeptidve use, hypothryoid, RA, DM
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carpal tunnel contains
The carpal tunnel is formed by:
Carpal bones (dorsal)
Transverse carpal ligament (flexor retinaculum) (ventral)
Contains:
Median nerve
Flexor digitorum superficialis/profundus tendons
Flexor pollicis longus tendon
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disc hernaitation
hard outer annulus fibrosis tears or weakens allowing the inner nucleus pulopsus to buldge out and compress nerves
usually posterior (posterior longitudinal ligament)
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2 nerve root entrapment
sciatica and thoracic outlet syndrome
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sciatica
compress lumbosacral nerve roots L4-S3 from disc herniation usually
Runs through the greater sciatic foramen, beneath the piriformis, down the posterior thigh, and branches into the tibial and common fibular nerves
Clinical Features:
Sharp, shooting, or burning pain radiating from lower back or buttock → down posterior thigh and possibly to calf/foot
Often unilateral
May be associated with:
Numbness/tingling (paresthesias)
Muscle weakness
↓ Reflexes (e.g., ankle jerk if S1 involved)
Pain worsened by sitting, bending, coughing
positive straight leg raise test
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thoracic outlet syndrome
compression of brachial plexus via scalenes (between collarbone and first rib)
but subclavian artery and vein also go through
nerve: pain, numb, weak
venous: arm swelling, cyanosis, venous thrombosis,
arterial: arm ischemia, pallor, weak pulse
esp from repetitive overhead arm activities
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thoracic outlet anatomy
Boundaries include:
First rib (inferiorly)
Clavicle (anteriorly)
Scalene muscles (anterolaterally)
Structures passing through:
Brachial plexus (C5–T1 nerve roots)
Subclavian artery and vein
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trigeminal neuralgia
sudden, severe, electric shock–like or stabbing facial pain in the distribution of the trigeminal nerve (cranial nerve V).
usually from vascular compression of the nerve or tumors
unilateral, paroxysmal, severe face pain
tic douloureux: externe, electric and intermittent pain
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peripheral neuropathy
🔹 Causes:
Diabetes mellitus (most common cause of polyneuropathy)
Alcoholism
Vitamin deficiencies (B12, B1, B6, E)
Toxins/medications (chemotherapy, heavy metals)
Infections (HIV, Lyme disease, leprosy)
Autoimmune diseases (Guillain-Barré syndrome, CIDP)
Hereditary (Charcot-Marie-Tooth disease)
Metabolic/endocrine disorders (hypothyroidism, renal failure)
🔹 Clinical Features:
Sensory symptoms: numbness, tingling, burning, pain, loss of proprioception
Motor symptoms: weakness, muscle wasting, fasciculations
Autonomic symptoms: orthostatic hypotension, gastroparesis, bladder dysfunction
Symmetric “stocking-glove” distribution common in polyneuropathy
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types of peripheral neuropathy
Mononeuropathy: Single nerve affected (e.g., carpal tunnel syndrome)
Mononeuritis multiplex: Multiple individual nerves affected in an asymmetric pattern
Polyneuropathy: Diffuse, symmetric nerve involvement (most common pattern)
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blepharitis
infalmmed eyelid margins
i.e. from bacterial or seborrheic dermatitis
burning, erythema, photophobia, flaking or crusting
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cataract
opacity or clouding of the lens
sx:
Gradual, painless decrease in vision
Glare and halos around lights
Difficulty with night vision
Absent red reflex on eye exam
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conjunctivitis
infalmmed eyelid
from non neisseria bacteria (i.e. chemicals or irritants, staph, strep, adenovirus, allergies) = pink eye
viral (watery, contagious), bacterial (purulent), allergic (itchy, bilateral), or chemical. Most cases resolve with supportive care or topical antibiotics.
🔹 Red Flag Organisms:
Neisseria gonorrhoeae: Hyperacute purulent discharge; can perforate cornea
Chlamydia trachomatis: Neonatal conjunctivitis (5–14 days after birth); also causes trachoma in endemic regions
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glaucoma
optic nerve damage and progressive visual field loss, often associated with increased intraocular pressure (IOP). (problem of flow of aqueous humor from posterior to anterior chamber increases the pressure)
most common is primary open angle;; decrease draining from trabecular meshwork from obstruction
--> gradual bilateral visual loss, blurry, no pain
primary angle closure is a medical emergency;; iris gets displaced forward
--> red, pain, dilated pupil
risks: DM, HTN etc
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uveitis/iritis/retinitis
iris; eye pain, photoprhobia, redness
retinitis: painless vision loss, floaters, field defects
usually from systemic disease
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keratitis
corneal inflammation ; infectious or non infectious
sx:
Eye pain
Photophobia
Red eye
Foreign body sensation
Tearing or discharge
Decreased visual acuity
Possible corneal opacity or ulcer on exam
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macular degeneration
leads to central vision loss (slow, painless, bilateral)
Dry macular degeneration is the more common type and progresses slowly. It is caused by the accumulation of drusen (yellow lipid deposits) beneath the retina, leading to gradual central vision loss. People often notice blurry or faded vision over time. It does not involve bleeding or fluid, and treatment focuses on AREDS2 vitamins, a healthy diet, and lifestyle changes like quitting smoking.
Wet macular degeneration is less common but more severe. It occurs when abnormal blood vessels grow under the retina and leak blood or fluid, causing sudden and rapid central vision loss. It often presents with distorted or wavy vision and dark spots. Treatment requires intravitreal anti-VEGF injections to stop the abnormal vessel growth and preserve vision.
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meunière disease
a chronic inner ear disorder characterized by recurrent episodes of:
Vertigo
Hearing loss
Tinnitus
A feeling of fullness in the affected ear
🔹 Cause / Pathophysiology:
Thought to be due to excess endolymphatic fluid in the inner ear → endolymphatic hydrops
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triad in Meniere's disease
Episodic vertigo (lasts minutes to hours, not positional)
Sensorineural hearing loss (typically unilateral and fluctuating)
Tinnitus (ringing or buzzing in ear) ± ear fullness or pressure
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treatment for Menieres disease
(endolymph buildup in inner ears)
low sodium diet, diuretics
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otitis externa (swimmers ear)
infection or inflammation of the external auditory canal, often caused by bacteria or fungi, typically following moisture exposure (swimming, q tips)
🔹 Clinical Features:
Ear pain (especially with movement of the tragus or pinna)
Itching in the ear canal
Discharge (clear, purulent, or foul-smelling)
Hearing loss (conductive, if canal is swollen or blocked)
Redness and swelling of the ear canal
Tenderness on palpation of the outer ear
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acute otitis media vs otitis media with effusion
Acute Otitis Media (AOM) is a painful, febrile middle ear infection with a bulging, inflamed tympanic membrane, often treated with antibiotics.
Otitis Media with Effusion (OME) is the presence of non-infected fluid in the middle ear, causing hearing loss without pain or fever, and usually resolves on its own.
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conductive vs sensorineural hearing loss
Conductive hearing loss is caused by blockage or damage in the outer/middle ear and improves with louder sounds, while sensorineural hearing loss results from inner ear or nerve damage, causing permanent difficulty with sound clarity.
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weber and rinne for conductive and sensorineural hearing loss
sensorineural (inner ear):
Weber test: Lateralizes to the unaffected (good) ear
Rinne test: Air conduction > bone conduction (normal
conductive (middle or outer ear)
Weber test: Lateralizes to the affected ear
Rinne test: Bone conduction > air conduction (abnormal)
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otitis media
🔹 Types:
Acute Otitis Media (AOM): Active infection with pain, fever, and inflamed tympanic membrane.
Otitis Media with Effusion (OME): Presence of fluid in the middle ear without signs of acute infection. Often follows AOM or eustachian tube dysfunction.
🔹 Etiology:
Common bacterial pathogens:
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Often preceded by viral upper respiratory infection.
🔹 Clinical Features:
Ear pain (otalgia)
Hearing loss (conductive)
Fever (more common in AOM)
Bulging, red tympanic membrane (AOM)
Possible otorrhea if perforation occurs
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vestibulitis
infect anterior portion of nostrils
risk: staph aureus
throbbing pain, bleeding, nodules
