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UWORLD REVIEW > UWorld > Flashcards

UWorld Flashcards

1
Q

What is an indication for prophylactic administration of anti-D Ig for RhD - patients

A
  • <72 hours after delivery of RhD + infant
  • <72 hours after spontaneous abortion
  • ectopic pregnancy
  • threatened abortion
  • 2nd/3rd trimester bleeding
  • at 28-32 weeks gestation
  • hydatidiform mole
  • chorionic villus sampling, amniocentesis
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2
Q

What labs/studies are performed during a initial prenatal visit?

A
  • CBC
  • Blood antibody and Rh typing
  • Pap smear
  • gonorrhea/chlamydia screening
  • urinalysis
  • RPR/VDRL
  • rubella and varicella antibody titer
  • hep B surface antigen
  • HIV screening
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3
Q

What labs/studies done at 16-18 weeks prenatal screening?

A

Quadruple screening (AFP, hcG, unconjugated estriol, maternal serum inhibin A)

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4
Q

What condition has the following quadruple screen results: AFP low, estriol low, hCG high, inhibin A high

A

Down syndrome

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5
Q

What test is done at 18-20 weeks prenatal screening

A

Anatomy scan to check for gross fetal abnormalities

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6
Q

What test is done at 24-28 weeks prenatal screening

A

1 hr glucose challenge to screen for GDM

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7
Q

What study/test is done at 32-37 weeks prenatal visit?

A
  • Gonorrhea/chlamydia cervical culture
  • group B strep testing
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8
Q

What is the mnemonic for vaccine schedule for pediatric population

A

Birth- Hep B
2mo- Hep B, Rota, DTaP, HiB, PCV, IPV
4mo- Rota, DTaP, HiB, PCV, IPV
6mo- Hep B, Rota, DTaP, HiB, PCV, IPV
12mo- Varicella, MMR, Hep A, DTaP, HiB, IPV, PCV
4-6yr- Varicella, DTaP, IPV, MMR

B
B DR HIP
DR HIP
B DR HIP
Very MAD HIP-ster
Very DIM

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9
Q

What is the most common primary malignant tumor that is more common in adolescents?

A

Osteosarcoma

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10
Q

What are the risk factors for osteosarcoma

A

Paget disease of bone, p53 genetic mutations, familial retinoblastoma, radiation exposure, bone infarcts

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11
Q

What regions do osteosarcoma involve

A

Proximal tibia, proximal humerus, distal femur

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12
Q

How does osteosarcoma present clinically and what are the labs and imaging for it

A

Presents as deep bony pain
Labs- high alk phos, high ESR, high LDH
Dx- biopsy of bone
Imaging- x ray shows sunburst pattern and Codman triangle, chest CT commonly done to check for metastases

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13
Q

Treatment for osteosarcoma

A

Radical surgical excision, chemotherapy

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14
Q

What is a highly malignant cartilage tumor occurring in the diaphysis of long bones and is most common in children

A

Ewing sarcoma

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15
Q

How does Ewing sarcoma present clinically and what are labs and imaging for it show

A

Ewing sarcoma presents as bony pain, tissue swelling, fever, fatigue, fractures with minor trauma
Labs- high WBCs, low Hgb, high ESR
dx- biopsy
Radiology- large destructive lesions, onion skinning of bone

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16
Q

Treatment for osteosarcoma

A

radiation, adjuvant chemo, radical excision

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17
Q

What is the most common benign bony tumor in metaphysis of long bone

A

Osteochondroma

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18
Q

How does osteochondroma present and where is it commonly found

A

Presents as irritated soft tissue overlying mass, palpable hard mass

Occurs in lower femur or upper tibia

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19
Q

What does osteochondroma show on imaging

A

bony growth off metaphysis of long bone, cancellous portion of long bone continuous with interior of lesion

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20
Q

Treatment for osteochondroma

A

None, unless causing soft tissue irritation or neurovascular compromise or continued growth occurs (surgery)

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21
Q

What appears as sclerotic cortical lesion on imaging with a central nidus of lucency

A

Osteoid osteoma

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22
Q

How does osteoid osteoma present and how is it treated

A

Presents as pain worse at night and unrelated to activity

Treated with NSAIDS

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23
Q

What is the cause of sheehan syndrome

A

Obstetric hemorrhage complicated by hypotension
- causes postpartum anterior pituitary infarction

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24
Q

What are the clinical features of sheehan syndrome

A
  • lactation failure (low prolactin)
  • amenorrhea, hot flashes, vag atrophy (low FSH and LH)
  • fatigue and brady (low TSH)
  • anorexia, weight loss, hypotension (low ACTH)
  • low lean body mass (low GH)
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25
Q

How do you diagnose Sheehan syndrome- what hormone levels do you check

A

Cortisol
Thyroxine
FSH
Prolactin

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26
Q

How do you treat Sheehan syndrome

A

Corticosteroids
Estrogen-progestin replacement therapy

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27
Q

Damage to endometrial basalis layer with D&C causes intrauterine adhesions and subsequent amenorrhea in what condition

A

Asherman syndrome

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28
Q

What causes acute adrenal insufficiency (adrenal crisis)

A
  • Adrenal hemorrhage or infarction
  • illness/injury/surgery
  • pituitary apoplexy
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29
Q

What are the clinical features of adrenal insufficiency

A
  • hypotension and shock
  • nausea, vomiting, abdominal pain
  • fever, generalized weakness
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30
Q

How do you treat adrenal crisis

A
  • hydrocortisone or dexamethasone
  • rapid IV volume repletion
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31
Q

Primary Adrenal Insufficiency vs Secondary Adrenal Insufficiency vs Tertiary Adrenal Insufficiency

A

1- due to impairment of adrenal glands (Addisons disease)
2- caused by impairment of pituitary gland
3- due to hypothalamic disease and decrease in CRF (corticotropin releasing factor)

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32
Q

Lab values in 1 vs 2 vs 3 adrenal insufficiency

A

1- low cortisol, low DHEAS, low androgens, high CRH, high ACTH
2- low cortisol, low DHEAS, low ACTH, high CRH
3- low cortisol, low DHEAS, low ACTH, low CRH

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33
Q

Causes of 1 adrenal insufficiency

A

Autoimmune > TB
drugs, infarction, hemorrhage, infiltration

SYMPTOMS
Salt cravings (because of low aldosterone)
Low libido (low androgens)
Low blood pressure
High melanin (hyperpigmentation)

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34
Q

Causes of 2 adrenal insufficiency

A

Adenoma, surgery, radiation, autoimmune

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35
Q

Symptoms of 2 adrenal insufficiency

A

Bitemporal hemianopsia is sometimes seen

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36
Q

What is the name of a rash that is described as diffuse red skin

A

Erythematous rash

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37
Q

Common febrile/toxic etiologies of erythematous rash

A

TEN (toxic epidermal necrolysis)
SSSS (staphylococcal scalded skin syndrome)
TSS (toxic shock syndrome)
Kawasaki (Pediatrics)
Scarlet Fever

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38
Q

Common afebrile erythematous rashes

A

Allergic reaction/ anaphylaxis
TEN (can be febrile or afebrile)

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39
Q

Macules (flat, red splotches) and papules (solid and raised) rash

A

Maculopapular rash

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40
Q

Common febrile/toxic maculopapular rashes

A

Viral exanthem (most common)
Lyme disease
RMSF
Meningococcemia
Syphilis
SJS
Erythema Multiforme

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41
Q

Afebrile etiologies of maculopapular rash

A

Drug reaction
Pityriasis Rosea
Scabies
Eczema
Psoriasis

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42
Q

Small, red (blood leak from capillaries), no blanching, may start in dependent areas

A

Petechial Rash

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43
Q

Febrile/toxic causes of petechial rash

A

Palpable:
RMSF
Meningococcemia
Endocarditis
Disseminated Gonoccoal

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44
Q

Afebrile Petechial Rash

A

ITP

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45
Q

Petechiae >0.5cm, no blanching, may be palpable

A

Pupuric rash

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46
Q

Common febrile/toxic causes of pupuric rash

A

Palpable: HSP
Non palpable: DIC, TTP

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47
Q

Afebrile causes of purpuric rash

A

TTP
Autoimmune vasculitis

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48
Q

Fluid filled lesions, vesicles <1cm, bullae >1cm

A

Vesiculobullous rash

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49
Q

Common febrile/toxic causes of vesiculobullous rashes

A

Disseminated:
varicella
smallpox
disseminated gonoccus
DIC

Localized
Hand, food and mouth
necrotizing fascitis

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50
Q

Afebrile causes of vesiculobullous rash

A

Diffuse:
Pemphigus vulgaris
Bullous pemphigoid

Localized:
Herpes zoster
Burns
Contact dermatitis

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51
Q

ITP symptoms

A
  • thrombocytopenia (isolated low platelets)
  • petechiae (non blanching red spots)
  • can have bleeding from gums
  • otherwise systemically well
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52
Q

ITP is commonly seen in what population

A

often in children
viral prodrome about 3 weeks prior

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53
Q

Treatment for acute ITP

A

Self limiting
IVIG/Steroids for active bleeding
platelet transfusion for life threatening bleeding

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54
Q

TTP symptoms

A

Neuro symptoms (AMS, seizure, stroke)
Fever
Hemolytic anemia
Thrombocytopenia
Renal involvement (proteinuria/renal failure)

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55
Q

TTP diagnosis

A

subendothelial and intraluminal deposits of fibrin and platelet aggregates in capillaries and arterioles (thrombotic events)

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56
Q

Treatment for TTP

A

consult hematology
plasma exchange with FFP

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57
Q

How is a pleural effusion described or is diagnosed on chest x ray

A

Pleural effusion is the accumulation of excess fluid between the layers of the pleura
- can present as shortness of breath, chest pain, cough

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58
Q

Pleural effusion on chest x-ray

A

pleural effusions appear white, contrasting with the air space which looks black
- small effusions are seen as a meniscus of increased density at the costophrenic angle
- large volume effusions cause pressure on the adjacent lung leading to collapse
- if the volume of effusion is greater than the degree of collapse, there will be accompanying mediastinal shift

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59
Q

What is transudative pleural effusion

A

Imbalance in the production and removal of pleural fluid due to systemic factors like heart failure or liver disease

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60
Q

What is exudative pleural effusion

A

Arising due to inflammation or damage to the pleura or nearby organs

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61
Q

Common causes of transudative pleural effusion

A

CHF
Cirrhosis
Nephrotic Syndrome
Atelectasis
peritoneal dialysis

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62
Q

Exudative Causes of Pleural Effusion

A

Pneumonia
Malignancies (cancer)
Tuberculosis
Pulmonary Embolism
Autoimmune Disorders (SLE, RA)
Pancreatitis (inflammation of pancreas can lead to fluid build up in pleural space)
Trauma (hemothorax or pneumothorax)

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63
Q

How do you treat a small pleural effusion

A

Observation

If pleural effusion is small and asymptomatic- just monitor

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64
Q

How do you treat large pleural effusions

A

For large effusions causing SOB, use thoracentesis to remove the fluid

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65
Q

What is lights criteria?

A

Pleural effusion is EXUDATIVE if
pleural fluid protein/serum protein >0.5
pleural fluid LDH/serum LDH >0.6
pleural fluid LDH is >2/3 upper limit of lab normal value for serum LDH

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66
Q

What does purulent pleural fluid indicate

A

Infection

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67
Q

What does bloody pleural fluid indicate

A

Malignancy, PE or trauma

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68
Q

What is the most common renal malignancy in children in ages 2-5

A

Wilms tumor (nephroblastoma)

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69
Q

What does WAGR stand for in association with nephroblastoma

A

WAGR
W- Wilms tumor
A- Aniridia
G- Genitourinary abnormalities
R- mental Retardation

Beckwieth-Wiedemann Syndrome
Denys Drash Syndrome

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70
Q

How does a nephroblastoma present

A

Usually asymptomatic
Unilateral abdominal mass
+/- abdominal pain, hypertension, hematuria

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71
Q

How do you treat nephroblastoma

A

Surgical excision
Chemotherapy
+/- radiation therapy

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72
Q

How do you diagnose Wilms tumor

A

Abdominal ultrasound 1st to differentiate Wilms tumor from other abdominal masses

Contrast- enhanced CT or MRI 2nd to evaluate the extent of the mass

CT of chest to identify pulmonary mets

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73
Q

What is a neuroblastoma

A

Tumor of neural crest cell origin that may arise in adrenal glands or sympathetic ganglia

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74
Q

What are risk factors for neuroblastoma

A

Neurofibromatosis
Tuberous Sclerosis
Pheochromocytoma
Beckwieth-Wiedemann Syndrome
Turner Syndrome

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75
Q

How does a neuroblastoma present clinically

A

abnormal distention and pain
weight loss
malaise
bone pain
diarrhea
abdominal mass
possible Horner syndrome and proptosis

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76
Q

What lab findings are seen with neuroblastoma

A

Possible increased vanillymandellic and homvanillic acids in 24hr urine collection used to detect catecholamine secreting tumors like NEUROBLASTOMA

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77
Q

What is 5-HIAA test used to diagnose

A

Carcinoid Syndrome

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78
Q

Symptoms of Carcinoid Syndrome

A

Serotonin secreting tumors- flushing, diarrhea, wheezing, heart problems

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79
Q

How is a neuroblastoma diagnosed

A

CT may locate adrenal or ganglion tumor

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80
Q

How is neuroblastoma treated

A

surgical resection
chemotherapy
radiation

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81
Q

When does erythema toxicum neonatorum present

A

birth to 3 days of age

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82
Q

What is the name of a benign neonatal rash that is described as pustules with erythematous base on trunk and proximal extremities

A

Erythema toxicum neonatorum

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83
Q

How do you treat erythema toxicum neonatorum

A

Observation
Usually resolves within a week

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84
Q

When do milia present

A

Birth

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85
Q

Firm white papules on face benign neonatal rash

A

Milia

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86
Q

How do you treat milia

A

Observation
Resolves within a month

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87
Q

Erythematous papular rash on occluded and intertriginous areas at any age (not at birth)

A

Miliaria rubra

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88
Q

Treatment for miliara rubra

A

Avoid overheating
If severe, topical corticosteroid

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89
Q

Nonerythematous pustules that evolve int hyperpigmented macules with collarette of scale

Diffuse, may involve palms and soles

A

Neonatal pustular melanosis

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90
Q

What is the treatment for neonatal pustular melanosis

A

Observation
Pustules resolve within days
Hyperpigmentation may last months

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91
Q

Erythematous papules and pustules on face and scalp only that appear around 3 weeks of age

A

Neonatal cephalic pustulosis

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92
Q

Treatment for neonatal cephalic pustulosis

A

Observation
Resolves in weeks to months
If severe, topical corticosteroid or ketoconazole

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93
Q

What is the ectopic implantation of endometrial glands

A

Endometriosis

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94
Q

What disease presents as dyspareunia, dysmenorrhea, chronic pelvic pain, infertility, dyschezia, cyclic dysuria, hematuria

A

Endometriosis

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95
Q

Physical examination findings of endometriosis

A

immobile uterus
Cervical motion tenderness
adnexal mass
rectovaginal septum, posterior cul-de-sac, uterosaral ligament nodules

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96
Q

How do you diagnose endometriosis

A

Direct visualization and surgical biopsy

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97
Q

What is the treatment for endometriosis

A

Oral contraceptive pills
NSAIDs
surgical resection

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98
Q

Inflammation inside the uterine cavity that can cause infertility by creating intrauterine adhesions that prevent pregnancy implantation

A

Endometritis

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99
Q

What are the symptoms of endometritis e

A

Commonly occurs after childbirth or miscarriage or cervical/uterine surgery (C-section)

Presents as fever, pelvic pain, vaginal bleeding or discharge, constipation, swelling in your abdomen

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100
Q

Benign growth of endometrial glands and stroma that present with painless intermenstrual spotting

A

Endometrial polyps

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101
Q

Heavy prolonged menstrual bleeding

A

Submucosal fibroids

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102
Q

Uterine fibroids are also known as

A

Uterine leiomyoma

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103
Q

Benign uterine masses composed of smooth muscle within myometrium, regress after menopause usually

A

Leiomyoma

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104
Q

Risk factors for leiomyoma

A

nulliparity
AA heritage
diet high in meats and alcohol
family hx

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105
Q

Leimyoma symptoms

A

possible menorrhagia, pelvis pressure or pain, palpable mass on examination

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106
Q

Imaging for leiomyoma

A

Transvaginal US or hysteroscopy

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107
Q

Treatment for uterine leiomyoma

A

Follow asymptopmatic fibroids with US to detect abnormal growth

GnRH agonists to reduce uterine bleeding and fibroid size

Myomectomy for resection of symptomatic fibroids in women wishing to maintain fertility

Hysterectomy in patients whose fertility is not a concern

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108
Q

Lining of uterus grows into walls of uterus

A

uterine adenomyosis

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109
Q

symptoms of adenomyosis

A

heavy menstrual period, pelvic pain, discomfort during sex

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110
Q

Treatment for adenomyosis

A

NSAIDS to soothe menstrual cramps
OCPs to lighten flow
IUD to help cramps and flow

Surgery - endometrial ablation, uterine artery embolization (affects fertility), hysterectomy

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111
Q

Rapid onset of periumbilic pain (severe) that is out of proportion to examination findings and late presentation of hematochezia

A

Acute mesenteric ischemia

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112
Q

Risk factors for acute mesenteric ischemia

A

Atherosclerosis
Embolic source (thrombus, cardiac vegetation)
Hypercoagulable disorder

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113
Q

Lab findings for AMI

A

leukocytosis
elevated amylase and phosphate level
metabolic acidosis

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114
Q

Diagnosis for Acute mesenteric ischemia

A

CT (preferred) or MR angiography

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115
Q

Age >50, bilateral pain and morning stiffness > 1 month, involving 2 of the following (neck or torso, shoulder or proximal arms, proximal thigh or hip, constitutional symptoms)

A

Polymyalgia rheumatica

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116
Q

PE findings on polymyalgia rheumatic

A

decreased active ROM in shoulders, neck and hips

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117
Q

Lab values in PMR polymyalgia rheumatica

A

High ESR
High CRP
normocytic anemia

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118
Q

Tx for polymyalgia rheumatica

A

Oral glucocorticoids (low dose- prednisone 10-20mg)

vs high dose glucocorticoids for patients with suspected GCA

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119
Q

SLE immunologic markers

A

ANA
Anti-dsDNA
Anti-Sm Ab
False positive RPR or VDRL

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120
Q

Immunologic markers for drug induced lupus

A

Antihistone antibodies
ANA

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121
Q

Immunologic markers for RA

A

RF
Anticitrullinated peptide antibodies (>90% specific)
ANA
HLA-DR4 common

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122
Q

Immunologic markers for polymyositis or dermatomyositis

A

ANA
Anti-Jo 1 antibodies in patients with interstitial lung disease

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123
Q

Immunologic marker for ankylosing spondylitis

A

HLA-B27

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124
Q

Immunologic markers for scleroderma

A

Anti-scl 70 ANA

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125
Q

immunologic markers for CREST syndrome

A

anticentromere antibodies

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126
Q

Immunologic markers for Sjogren syndrome

A

Anti-Ro (anti SSA) ANA
Anti-La (anti SSB) ANA

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127
Q

Rheumatoid arthritis causes

A

Autoimmune disease- leads to inflammation and joint damage

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128
Q

RA symptoms

A

Affects small joints in hands and feet
morning stiffness lasting >1hr, low fevers, rheumatoid nodules

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129
Q

RA risk factors

A

female
smoking
exposure to dangerous chemicals like asbestos or silica

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130
Q

OA causes

A

wear and tear on your joint cartilage causing cartilage break down due to daily use and aging

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131
Q

OA symptoms

A

Affects joints you use most (hands and spine) and weight bearing joints (hips and knees)

Pain, stiffness, swollen joints, joint noises during movement

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132
Q

OA risk factors

A

genetic
excess weight
older age, joint injury, overuse of joints

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133
Q

OA treatment

A

NSAIDs
non medicinal relief (hot or cold packs)

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134
Q

RA treatment

A

DMARDs (disease modifying antirheumatic drugs)- suppress immune system and reduce inflammation

Traditional DMARDs - methotrexate, sulfasalazine, hydroxychloroquine, leflunomide, azathioprine

Biologic DMARDs- target specific modules, cells and pathways causing inflammation

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135
Q

ALS tracts affected and symptoms

A

Corticospinal tract and ventral horn affected

Symptoms- spastic and flaccid paralysis (UMN and LMN symptoms)

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136
Q

Poliomyelitis tracts affected and symptoms

A

Ventral horn affected

Symptoms- flaccid paralysis (LMN lesion)

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137
Q

Tabes dorsalis tracts affected and symptoms

A

Dorsal columns affected

Symptoms- impaired proprioception and pain

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138
Q

Spinal artery syndrome tracts affected and symptoms

A

Corticospinal tract, spinothalamic tract, ventral horn, lateral gray matter affected- DORSAL COLUMNS SPARED

Symptoms-
bilateral loss of pain and temperature one level below lesion

bilateral spastic paresis (below lesion)

bilateral flaccid paralysis (level of lesion)

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139
Q

Vit B12 def tracts affected and symptoms

A

Dorsal columns and corticospinal tract

Symptoms- bilateral loss of vibration and discrimination and bilateral spastic paresis affecting legs before arms

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140
Q

Syringomyelia tracts affected and symptoms

A

Ventral horn

Symptoms- bilateral loss of pain and temperature one level below lesion and bilateral flaccid paralysis at level of lesion

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141
Q

Brown Sequard Syndrome tracts affected and symptoms

A

all tracts on one side of cord affected

Symptoms- ipsilateral loss of vibration and discrimination
ipsilateral spastic paresis
ipsilateral flaccid paralysis
contralateral loss of pain and temeparature

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142
Q

UMN symptoms

A

Hypertonic, spastic paralysis, hyperreflexia, Babinski sign (upgoing plantars)

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143
Q

LMN symptoms

A

Hypotonia, flaccid paralysis, fasciculations, downgoing plantars (absent Babisnki)

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144
Q

Post Op Fever Days 1-2

A

Wind

  • atelectasis #1
  • pneumonia

Diagnosis - CXR, sputum culture if pneumonia is suspected
Tx- incentive spirometry, antibiotics (vanc + pip/tazo)

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145
Q

Post Op Fever Days 3-5

A

Water

UTI
Dx- urinalysis (nitrite and leukocyte esterase +)
Tx- antibiotics

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146
Q

Post op Fever Days 5-6

A

Walking

DVT
Thrombophlebitis (IV site infection)

Dx- Doppler US
Tx- anticoagulation- heparin then warfarin
Replace IVs

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147
Q

Post Op Fever Day 7

A

Wound

Incision Site wound
Infectious Cellulitis

Dx- physical exam: erythema, pus, swelling
Tx- abscess incision/drainage, antibiotics

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148
Q

Post Op Fever Day 8-15

A

Wonder Drugs

Drug Reaction
Deep Abscess

Dx- D/C likely medication, CT scan
Tx- drainage of abscess

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149
Q

Tuberculosis Symptoms

A

Chronic cough >3 weeks
weight loss
night sweats
fatigue
sometimes hemoptysis
can affect other organs- pleuritic chest pain, neuro symptoms in TB meningitis

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150
Q

Pneumonia symptoms

A

Sudden onset of high fever
productive cough with yellow or green sputum
Chest pain
SOB
Fatigue

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151
Q

Common causes of TB

A

Mycobacterium tuberculosis cause
- spreads through airborne droplets when infected person coughs or sneezes

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152
Q

Pneumonia causes

A

Commonly bacteria (S. pneumo)
Viruses (flu, RSV)

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153
Q

Imaging findings for TB

A

Irregular patches (lesions) in lungs especially in upper lobes
Cavitation is a characteristic feature
TB infections tends to start in the top of the lungs

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154
Q

Pneumonia imaging features

A

Consolidated areas (infiltrates) in the lungs typically in the lower lobes

Effusions can also be seen

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155
Q

Diagnosis for TB

A

Skin test (tuberculin test
Blood test
Chest x ray for characteristic lesions
Sputum test to detect TB in mucus

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156
Q

Diagnosis for pneumonia

A

Chest X ray to see infiltrates
Blood test to assess inflammation and infection markers

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157
Q

TB treatment

A

latent TB: treated with isoniazid for 3-4 months active TB: RIPE protocol (rifampin, isoniazid, pyrazinamide, ethambutol)

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158
Q

Pneumonia Treatment

A

antibiotics specific to causative agent
Supportive care

159
Q

Primary Hyperaldosteronism (CONN SYNDROME) causes

A

Caused by issues within the adrenal glands
- Adrenal adenomas (benign tumors)
- Bilateral Adrenal Hyperplasia (enlargement of both adrenal glands)

160
Q

Secondary Hyperaldosteronism causes

A

Occurs due to problems outside of the adrenal glands (reduced kidney blood flow, heart failure, liver cirrhosis)

  • activation of RAAS secondary to perceived low blood pressure in the kidneys (renal artery stenosis, heart failure, cirrhosis, nephrotic syndrome)
161
Q

Presenting symptoms of hyperaldosteronism

A

headache, weakness, paresthesia, recalcitrant HTN, tetany

162
Q

Lab findings in hyperaldosteronism

A

decreased K+ (because of high aldosterone)
metabolic alkalosis
mildly increased Na_
increased 24 hour urine aldosterone
high ratio of plasma aldosterone concentration to plasma renin activity (PAC: PRA) ratio indicated primary hyperaldosteronism

163
Q

Imaging findings for hyperaldosteronism

A

CT or MRI may detect adrenal mass

164
Q

Treatment for hyperaldosteronism

A

surgical resection of tumor (primary hyperaldosteronism)

treat underlying disorder causing RAA hyperactivity (secondary hyperaldosteronism)

aldosterone antagonists (spironolactone) improve hypokalemia until definitive therapy administered

165
Q

Primary Adrenal Insufficiency causes

A

mineralocorticoid (aldosterone) deficiency
glucocorticoid (cortisol) deficiency

caused by adrenal disease or ACTH insufficiency

166
Q

Addison Disease pathophysiology

A

Primary adrenal insufficiency
-autoimmune destruction of adrenal cortices caused by autoimmune disease

167
Q

Secondary corticoadrenal insufficiency causes

A

insufficient ACTH production by pituitary

168
Q

Tertiary corticoadrenal insufficiency causes

A

insufficient corticotropin releasing hormone (CRH) secretion by hypothalamus (commonly due to chronic corticosteroid use)

169
Q

Symptoms of adrenal insufficiency

A

weakness
fatigue
anorexia
weight loss
nausea and vomiting
arthralgias
decreased libido in women
memory impairment
depression
HYPOTENSION
possible INCREASE IN SKIN PIGMENTATION

170
Q

Lab values in adrenal insufficiency

A

Low Na+ and high K+ due to low aldosterone, eosinophilia and decreased cortisol

High ACTH with Addison disease
Low ACTH with secondary or tertiary insufficiency

Low cortisol that increases following ACTH analog (cosyntropin) administration in secondary or tertiary insufficiency but not in Addison disease

171
Q

Treatment for adrenal insufficiency

A

Treat underlying disease

Glucocorticoid replacement (hydrocortisone, dexamethasone, prednisone)

Mineralocorticoid replacement

DHEA

hydration to achieve adequate volume status

172
Q

Complications of adrenal insufficiency

A

Addisonian crisis- severe weakness, fever, mental status changes, vascular collapse caused by stress and increased cortisol need
- treat with IV glucose and hydrocortisone or vasopressors

173
Q

Causes of Hematuria

A

Nephrolithiasis
UTI
BPH
Bladder Inflammation (cystitis)
Kidney disease
Trauma or injury
Endometriosis
Sickle Cell Disease

174
Q

Bladder Cancer epidemiology and population at risk

A

> 90% risk with urothelial carcinoma

High risk with smokers and exposure to industrial carcinogens

175
Q

Symptoms of bladder cancer

A

Painless hematuria throughout micturition
Irritative voiding symptoms (frequency, urgency, dysuria)
Regional pain

176
Q

Dx for bladder cancer

A

GOLD STANDARD- flexible cystoscopy with biopsy
Urine cytology

177
Q

Staging of bladder cancer

A

TURBT
Upper urinary tract imaging

178
Q

Tx for bladder cancer

A

No muscle invasion: TURBT and intravesical immunotherapy

Muscle invasion: radical cystectomy and systemic chemotherapy

metastatic bladder cancer- systemic chemotherapy and immunotherapy

179
Q

Nephritic Syndrome symptoms

A

Acute hematuria and proteinuria secondary to glomerular inflammation

Commonly see oliguria and gross hematuria

180
Q

Nephritic Syndrome labs

A

increased BUN
increased Cr
hematuria and proteinuria on UA
24 hr urine collection- protein <3.5g/day

181
Q

Nephrotic Syndrome symptoms

A

Significant proteinuria associated with hypoalbuminemia and hyperlipidemia

Edema
Foamy urine
Dyspnea
Hypertension
Ascites

182
Q

Nephrotic Syndrome labs

A

Decreased albumin and hyperlipidemia
proteinuria >3.5g/day seen on 24hr urine collection

183
Q

Nephritic Syndromes

A

PSGN
IgA nephropathy
Goodpasture Syndrome
Alport Syndrome
RPGN
Lupus nephritis
Wegener granulomatosis

184
Q

Nephrotic Syndromes

A

Minimal change disease
FSGN
Membranous nephropathy
MPGN
Diabetic Nephropathy
Amyloidosis

185
Q

PSGN pathology, symptoms, labs, treatment

A

PSGN- caused by Group A strep infection

Symptoms- recent infection, oliguria, edema, brown urine, hypertension, common in children

Labs- hematuria and proteinuria in UA, high ASO titer, subepithelial humps of IgG and C3 on renal basement membrane on electron microscopy

Treatment- self limited, supportive care

186
Q

IgA nephropathy (Berger disease) pathology, symptoms, labs, treatment

A

Deposition of IgA immune complexes in mesangial cells

Commonly few days after infection while PSGN is weeks after infection

symptoms- hematuria, flank pain, low grade fever

labs- high serum IgA, mesangial cell proliferation on electron microscopy

Tx- occasional self limited, ACE-I and statins for persistent proteinuria

187
Q

Goodpasture syndrome pathology, symptoms, labs, treatment

A

Pathology- deposition of antiglomerular and antialveolar basement membrane antibodies

Symptoms- dyspnea, hemoptysis, myalgias, hematuria

labs- serum IgG antiglomerular basement membrane Ab, anemia, LINEAR PATTERN OF IgG AB DEPOSITION

Tx- plasmapheresis, corticosteroids, immunosuppressive agents

188
Q

Alport Syndrome pathology, symptoms, labs, treatment

A

Hereditary defect in collage IV in basement membrane
Sx- hematuria, high frequency hearing loss, eye disease (CANT PEE, CANT SEE, CANT HEAR A BEE)

Labs- red cell casts, split basement membrane on electron microscopy

tx- ace-I may reduce proteinuria
renal transplant may be complicated by alport related development of goodpasture syndrome

189
Q

RPGN pathology, symptoms, labs, treatment

A

Rapidly progressive renal failure from idiopathic causes or associated with other glomerular diseases or systemic infection

sx- sudden renal failure, weakness nausea, weight loss, dyspnea, hemoptysis, myalgias, fever, oliguria

labs- deposition of inflammatory cells in Bowman capsule and crescent formation
- pauci immune RPGN is ANCA1

tx- poor prognosis, tx with corticosteroids plasmapharesis and immunosuppressives, renal transplant frequently required

190
Q

Lupus nephritis pathology, symptoms, labs, tx

A

Complication of SLE involving proilferation of endothelial and mesangial cells

sx- possible hypertension or renal failure

labs- ANA, Anti-DNA antibodies, hematuria and possible proteinuria

tx- corticosteroids or immunosuppressives
ace-I and statins to help reduce proteinuria

191
Q

Wegeners granulomatosis pathology, symptoms, labs, tx

A

Similar to crescentic disease with addition of pulm involvement- granulomatous inflammation of airways and renal vasculature

symptoms- weight loss, resp symptoms, hematuria, fever

labs- cANCA,, deposition of immune complexes in renal vessels on electron microscopy

tx- corticosteroids, cytotoxic agents (cyclophosphamide)

192
Q

Minimal change disease pathology, symptoms, labs, tx

A

Idiopathic cause, may involve effacement of podocytes on basement membrane

symptoms= possible HTN, increased frequency of infections, most common cause of nephrotic syndrome in children

labs- HLD, hypoalbuminemia, proteinuria, flattening of podocytes on electron microscopy

tx- corticosteroids

193
Q

FSGN pathology, symptoms, labs, tx

A

Associated with drug use of HIV, systemic sclerosis of glomeruli

Sx- possible HTN, most common cause of nephrotic syndrome in adults

Labs- HLD, hypoalbuminemia, hematuria, high proteinuria on UA, sclerotic changes in glomeruli

tx- corticosteroids, Ace-I, statins

194
Q

Membranous nephropathy pathology, sx, labs, tx

A

Idiopathic or associated with infection, SLE, neoplasm or drugs causes, thickening of basement membrane

Symptoms- edema, dyspnea, hx of infection or medication use, associated with Hep B and hep C

labs- HLD, hypoalbuminemia, proteinuria on UA, spike and dome basement membrane thickening on electron microscopy

tx- corticosteroids, ace-I, statins

195
Q

Membranoproliferative glomeruloneprhitis pathology, sx, labs, tx

A

idiopathic or associated with infection o autoimmune disease
thickening of basement membrane, associated with HepB and HepC, SLE< and subacute bacterial endocarditis

sx- edema, HTN, hx of systemic infection or autoimmune condition

labs- basement membrane thickening with double layer tram track appearance on electron microscopy

196
Q

Diabetic nephropathy pathology, sx, labs, tx

A

basement membrane and mesangial thickening related to diabetic vascular changes

sx- hx of DM, hypertension, progressive renal failure

labs- nephrotic symptoms, basement membrane thickening, round nodules (kimmelstein wilson nodules) in glomeruli

tx- treat underlying DM and dietary protein restriction, Ace-I and tight BP control

197
Q

Amyloidosis pathology, sx, labs, tx

A

Deposition of amyloid protein fibrils in glomeruli and/or renal vasculature, may also involve other tissues

Sx- edema, may progress to renal failure

labs- nephrotic symptoms, congo red stain of biopsy shows apple green birefringence on polarized light

tx- melphalan, hematopoietic stem cell transplant

198
Q

Unintentional
Inattentive
Distractible
Disorganized
Increased Motor Activity
2+ settings
>6 months of symptoms

A

ADHD

199
Q

Treatment for ADHD

A

Behavioral therapy first line

Atomoxetine or stimulant (methylphenidate, amphetamine) improve ability to focus and control behavior

Alpha 2 agonists and TCAs may be used in refractory cases

200
Q

Deceitful for gain
Violates others
Destructive
Intentionally breaks law
Truancy

A

Conduct disorder

201
Q

Conduct disorder < 18
What disorder >18

A

Antisocial personality disorder

202
Q

Treatment for conduct disorder

A

Psychotherapy, psychostimulants helpful when comorbid ADHD diagnosed, mood stabilizers in severe cases

203
Q

Sensitive/Touchy
Willful
Spiteful Vindictive
Defensiveness, excuse making, potential outbursts

A

Oppositional defiant disorder

204
Q

OCPs (combined) - side effects and ocntraindications

A

possible nausea, headache and bloating
increased risk for DVT
contraindicated in heavy smokers, previous hx of DVT, estrogen related cancer, liver disease or hypertriglyceridemia

205
Q

Progestin only OCP side effects

A
  • used if pt has contraindication for estrogen
  • can cause breakthrough bleeding
  • has to be taken at same time everyday
206
Q

Depo Provera shot

A
  • progestin analog every 3 months, inhibits ovulation and endometrial development
  • SE- nausea, headache, weight gain, osteoporosis, irregular bleeding
207
Q

Progestin Implant

A

subcutaneous implant that slowly releases progestin over 3 years

SE: irregular bleeding, breast pain

208
Q

Copper IUD

A

Object inserted into uterus by physician with slow release of copper to prevent fertilization and interfere with sperm production
- 10 years
can be placed soon after intercourse as emergency contraception

Risks- small risk of spont abortion or uterine perfortation and menorrhagia

209
Q

Progestin releasing IUD

A

Left in place for 5 years
- small risk of spont abortion and uterine perf

210
Q

Inflammation of cornea

A

Infectious keratitis

211
Q

Causes of infectious keratitis

A

Bacterial- staph, strep, pseudomonas
- central round ulcer, stromal abscess, mucopurulent discharge

Vital- HSV or herpes Zoster
- branched dendritic ulcerations, decreased corneal sensation, watery discharge, recurrent episodes

Fungi- candida
- ulcerations with feathery margins and satellite lesions, mucopurulent discharge, indolent course (vs acute course with bacteria)

Contaminated Water

212
Q

Symptoms of infectious keratitis

A

Eye redness, pain, blurred vision, excess tears, photophobia, difficulty opening your eyelid due to pain or irritation

213
Q

Lens dislocation (ectopia lentis)

A

Commonly caused by trauma- direct blow to eye or blunt trauma to head

Also Marfans Syndrome and homocystinuria

214
Q

Symptoms of lens dislocation

A

Painless vision loss
Tremulous iris with eye movement
lens displacement on slitlamp examination

215
Q

Marfan Syndrome symptoms

A

Caused by defective fibrillin which is an essential component of ligaments

Features
- unlike homocystinuria, has normal levels of homocysteine and methionine
- Ectopia lentis
- Characteristic marfanoid habitus (tall stature, increased arm to height ratio, joint hypermobility) not usually apparent in young children
- Scoliosis
- High myopia (nearsightedness)
- Aortic root disease (dilation, dissection) = major cause of morbidity and REQUIRES MARFAN PT TO GET ECHO

216
Q

Homocystinuria Symptoms

A

Caused by mutations in CBS (cystathionine beta synthase) which converts homocysteine into cysteine

  • high levels of homocysteine present
  • symptoms- lens dislocation, nearsightedness, long limbs and slender fingers, neuro complications, increased risk of blood clots

Tx- Vit B6

217
Q

Ehlers Danlos symptoms

A

Affects connective tissues in body
- causes joint hypermobility which can lead to joint dislocation
- stretchy, fragile and prone to bruising skin
- muscle pain and fatigue
heart valve problems and blood vessel fragility

218
Q

Mutation in COL5A1 or COL5A2 gene causes what condition

A

Ehlers Danlos (classic syndrome)

  • these genes encode proteins essential for forming Type V collagen
219
Q

12-18 month children stop breathing

A

Breath Holding Spells

220
Q

Cyanotic vs Pallid Breath Holding Spell

A

Cyanotic- child turns blue bc of lack of O2 in blood- provoked by emotional upset, last less than a minute

Pallid- child appears pale, resemble fainting, caused by sudden fright or minor pain, last longer than a minute

221
Q

Systemic sclerosis vs scleroderma

A

Scleroderma- thickening and hardening of skin due to excessive collagen production

Systemic sclerosis- scleroderma affects skin and internal organs

222
Q

Anti-topoisomerase (Scl-70) antibody seen in

A

diffuse systemic sclerosis and linked to lung involvement

223
Q

Anticentromere antibody seen in

A

More common in limited systemic sclerosis and is associated with elevated blood pressure in the pulmonary system

224
Q

Spur cell RBC (acanthocyte)

A

Irregular narrow base sharp projections of red cell membrane (spaced out projections)

  • seen in:
  • cirrhosis
  • abetalipoproteinemia
  • post splenectomy
  • microangiopathic hemolytic anemia (DIC, TTP, HUS)
225
Q

Burr Cell RBC (echinocyte)

A

regular broader-base short projections of red cell membrane

seen in:
- uremia (chronic liver disease)
- liver disease
- hyperlipidemia

226
Q

Bite cells (degmacytes)

A

Seen in oxidative hemolysis- G6PD deficiency - uncontrolled oxidative stress causes hemoglobin to denature and form Heinz bodies

227
Q

Schistocyte (helmet cell)

A

Seenin DIC, hemolytic anemia, frequently a consequence of mechanical artificial heart valves, HUS, TTP, MAHA

228
Q

Dacrocyte (teardrop cell)

A

Commonly seen in primary myelofibrosis, myelodysplastic syndromes

229
Q

SLE nephritis

A

presents as foamy urine, edema in legs ankles and face, high blood pressure, kidney dysfunction (elevated creatinine)

  • increases risk of B cell lymphoma
230
Q

Molar pregnancy/Hydatidiform Mole

A

Symptoms- vaginal bleeding, severe nausea and vomiting, uterine enlargement, rapidly rising hCG levels

Dx- hcG, transvaginal ultrasound

231
Q

Choriocarcinoma symptoms

A

Rare and aggressive cancer that develops from cells that were part of placenta during pregnancy - occurs in uterus or ovaries

symptoms:
Irregular vaginal bleeding
pelvic pain
if it spreads to other parts of body can cause coughing, trouble breathing, headaches, abdominal pain

dx- pelvic exam, blood test to measure hCG levels, liver function and kidney function, US, CT

tx- chemotherapy, surgery may be needed

232
Q

Lab values seen in choriocarcinoma

A

High levels of beta hCG
AFP is elevated
Elevated LDH levels can indicate tumor activity

233
Q

Fluid filled swelling behind the knee joint in the popliteal fossa

A

Bakers cyst- extension of synovial membrane

234
Q

Symptoms of bakers cyst

A

Visible bulge behind the knee, pain when bending or straightening knee, stiffness and limited range of motion

Dx- US and MRI
tx- aspiration of cyst fluid, cortisone injections into knee to reduce inflammation, self care

235
Q

Prepatellar Bursitis

A
  • located in prepatellar bursa
  • commonly known as housemaid’s knee
  • symptoms- pain, swelling and tenderness at front of the knee
  • causes- repetitive kneeling or direct trauma
236
Q

Pes anserine bursitis

A

affects bursae on the lower inner side of knee
- commonly seen in people who engage in activities like running or cycling

237
Q

Infrapatellar Bursitis

A
  • involves the bursae located just under the patella
  • due to overuse, repetitive movements or direct impact
238
Q

Suprapatellar Bursitis

A

Involves the bursae located just above the kneecap
- often seen in OA and RA

239
Q

Internal rupture of respiratory system, chest wall intact

A

Closed pneumothorax

240
Q

Types of closed pneumothorax

A

Spontaneous, COPD, TB, blunt trauma

241
Q

Passage of air through opening in chest wall

A

Open pneumothorax

242
Q

Types of open pneumothorax

A

Penetrating trauma, iatrogenic (central line placement, thoracentesis, biopsy)

243
Q

Open pneumothorax, ball valve” condition allows air to enter but not leave pleural space

A

Tension pneumothorax

244
Q

Unilateral chest pain, dyspnea, decreased chest wall movement, unilateral decreased breath sounds, increased resonance to percussion, decreased tactile fremitus, respiratory distress, hypotension

A

Pneumothorax

245
Q

Deviation of trachea

A

Tension PTX

246
Q

CXR of pneumothorax

A

lung retraction and mediastinal shift away from affected side
Tension PTX- shows tracheal deviation

247
Q

Diagnosis of PTX

A

CXR and ultrasound

248
Q

Tx of PTX

A

small PTX- supplemental O2
Large PTX- chest tube placement
open PTX with small wound- tx with chest tube and occlusive dressing
tension PTX- requires immediate needle decompression and chest tube placement

249
Q

Collection of blood in pleural space caused by trauma, malignancy, TB or pulmonary

A

Hemothorax

250
Q

CXR for hemothorax

A

resembles that for pleural effusion
blunting of costophrenic angles
upright CXR preferred

251
Q

Tx for hemothorax

A

supplemental O2
chest tube placement
thoracotomy recommended if there is drainage of >1500mL after initial chest tube insertion or continuous drainage of 200mL/hr over 4 hours

252
Q

Moderate abdominal pain and tenderness
Hematochezia, diarrhea
leukocytosis, lactic acidosis

A

Colonic ischemia

253
Q

Colonic ischemia pathophysiology

A

Nonocclusive, “watershed” ischemia
- due to underlying atherosclerotic disease
- state of low blood flow (hypovolemia)
- repair of AAA is a common precipitating event as patients are often older and have extensive atherosclerotic vascular disease

254
Q

Dx for colonic ischemia

A

CT scan- colonic wall thickening, fat stranding
Endoscopy: edematous and friable mucosa

255
Q

Tx for colonic ischemia

A

IV fluids and bowel rest
Antibiotics with enteric coverage
Colonic resection if necrosis develops

256
Q

Immature central respiratory center in preterm infants

A

Apnea of prematurity

257
Q

Clinical features of apnea or prematurity

A

Intermittent apnea (cessation of respiration for >20 seconds) start at age 2-3 days
- associated bradycardia and desaturation sometimes seen
- well-appearing in between episodes

258
Q

Tx for apnea of prematurity

A

Caffeine
Noninvasive ventilation
Resolves by expected due date

258
Q

Obstructive apnea caused by severe bronchopulmonary dysplasia

A

occurs after 28 days
causes chronic hypoxia
tx- dexamethasone and albuterol

258
Q

Premature infant with respiratory distress and normal CXR

A

apnea of prematurity
sepsis
intraventricular hemorrhage
hypoglycemia
hypothermia
narcosis

259
Q

Premature infant with respiratory distress and abnormal CXR

A

RDS
TTN (premature or full term)
Pneumonia
Pneumothorax
Congenital Abnormality

260
Q

Not premature baby with respiratory distress

A
  • Meconium aspiration- meconium in amniotic fluid
  • infectious- sepsis or pneumonia
  • non infectious- RDS, TTN, pneumothorax, congenital abnormality
261
Q

Cyanotic Heart Defects 5Ts

A

1 T- truncus arteriosus- one great vessel leaving heart
2 T- transposition of great arteries- pulmonary artery and aorta are transposed
3 T- tricuspid atresia- tricuspid valve fails to form
4 T- tetralogy of fallot - tetrad of cardiac defects- pulm stenosis, RVH, overriding aorta, VSD
5 T- total anomalous pulmonary venous return
5 words- pulmonary veins do not connect to left atrium

262
Q

Hyperacute transplant rejection time, etiology, morphology

A

minutes to hours after transplant
- caused by antidonor antibodies in recipient
- gross mottling and cyanosis, arterial fibrinoid necrosis and capillary thrombotic occlusion
- untreatable, should be avoided by proper cross matching

263
Q

Acute transplant rejection

A

occurs 6 days to 1 year after transplantation (usually <6 months)
- caused by antidonor T cell proliferation in recipient
- tx- frequently reversible through immunosuppressive agents

264
Q

Chronic transplant rejection

A

Occurs >1 year after transplantation
- caused by multiple cellular and humoral immune reactions to donor tissue
- morphology- vascular wall thickening and luminal narrowing, interstitial fibrosis and parenchyma atrophy
tx- immunosuppression may serve some role

265
Q

CMV colitis

A

occurs in patients with IBD, particularly those with steroid refractory colitis
- histology with immunochemistry for diagnosis
- tx- antiviral treatment

266
Q

Microscopic colitis

A

Inflammatory disorder characterized by chronic diarrhea
- detected through histologic evaluation with mucosal biopsy
- unlike UC, microscopic colitis requires microscopic evaluation of colon tissue samples
- sx- abdominal pain and frequent stools but not typically bloody or rectal bleeding

267
Q

Deceleration that begins near the onset of a uterine contraction with the lowest point occurring at the same time as the peak of the contraction

A

Early decelerations

268
Q

Cause of early decelerations

A

compression of fetus head during a uterine contraction
- harmless decelerations and do not affect fetal O2

269
Q

Deceleration that begins just after a contraction with the lowest point occurring after the peak of the contraction

A

Late decelerations

270
Q

Cause of late deceleration

A

uteroplacental insufficiency which reduces blood flow to the placenta- leading to decreased O2 and nutrient transfer to the fetus
- causes- maternal hypotension from epidural, dehydration, anemia, rapid uterine contractions, placental abruption, fetal hypoxia

271
Q

Decelerations that vary in shape, duration and intensity and don’t necessarily correlate with uterine contractions

A

Variable decelerations

272
Q

Cause of variable decelerations

A

umbilical cord compression
- if decelerations become repetitive, blood delivered to fetus can be reduced and cause fetal hypoxia and acidosis

273
Q

Side effects of second generation antipsychotics

A

metabolic syndrome- weight gain, dyslipidemia, hyperglycemia

highest risk drugs- clozapine and olanzapine

monitoring guidelines- BMI, fasting glucose and lipids, blood pressure, waist circumference

274
Q

Ischemic Hepatitis symptoms

A

aka shock liver
- characterized by acute liver injury caused by insufficient blood flow and insufficient oxygen delivery to the liver
- due to low blood pressure or shock but also due to blood clot in hepatic artery

sx- weakness, fatigue, mental confusion, low urine production
- jaundice or hepatic coma also possible

275
Q

Symptoms of primary sclerosing cholangitis

A

fatigue and pruritis with progressive disease
- associated with IBD, particularly UC

276
Q

Lab findings on Primary sclerosing cholangitis

A

cholestasis (high ALP, GGT, bilirubin)
multifocal strictures/dilation of bile ducts on MRCP

277
Q

Complications of PSC

A

cholangitis, cholangiocarcinoma, colon cancer
fat soluble vitamin deficiencies

278
Q

Acute Cholangitis symptoms

A

RUQ pain, fever, jaundice, hypotension, altered mental status (Reynolds pentad)
- commonly occurs due to infection of extrahepatic biliary system that usually occurs due to biliary obstruction which predisposes patients to bacterial invasion

279
Q

Symptoms of magnesium toxicity

A

Mild: nausea, flushing, headache, hyporeflexia
Moderate: areflexia, hypocalcemia, somnolence
Severe: respiratory paralysis, cardiac arrest

280
Q

Tx of magnesium toxicity

A

Stop magnesium
Give IV calcium gluconate

281
Q

Leakage of urine with coughing, sneezing, lifting

A

Stress incontinence
- caused by decreased urethral sphincter tone
- urethral hypermobility

282
Q

Sudden overwhelming urge to urinate

A

Urge incontinence
- detrusor overactvity

283
Q

Incomplete emptying and persistent involuntary dribbling

A

Overflow incontinence
- impaired detrusor contractility
- bladder outlet obstruction

284
Q

Pyogenic liver abscess symptoms

A

Fever, RUQ pain, leukocytosis, elevated liver function studies
- rounded hypoattenuating lesion in the liver

285
Q

Causes of pyogenic liver abscess

A

Direct extension from biliary tract infections
Penetrating trauma
hematogenous spread from the system (IE) or portal circulation (intrabdominal infection)

286
Q

Diagnosis of liver abscess

A

well defined hypoattenuating rounded lesion often surrounded by a peripherally enhancing abscess membrane on CT scan

287
Q

Treatment for liver abscess

A

Blood cultures
Antibiotics
PERCUTANEOUS ASPIRATION AND DRAINAGE- both diagnostic and therapeutic

288
Q

Symptoms of arthropathy of hereditary hemochromatosis

A

onset < 40
chronic pain and bony swelling
most common at 2nd and 3rd MCP joints
occasional acute flare

289
Q

X ray signs of arthropathy of hereditary hemochromatosis

A

joint space narrowing
chondrocalcinosis
hook-shaped osteophytes at metacarpal heads

290
Q

Treatment for arthropathy of hereditary hemochromatosis

A

NSAIDs
therapeutic phlebotomy

291
Q

What age does Hodkin lymphoma affect

A

Bimodal peak incidence: age 15-35 and >60
- association with EBV in immunosuppression

292
Q

Symptoms of Hodkins lymphoma

A

Painless lymphadenopathy
Mediastinal mass
B symptoms
Pruritis

293
Q

How do you diagnose hodgkin lymphoma

A

Lymph node biopsy
Reed Sternberg cells on histology

294
Q

Most common childhood cancer in ages 2-5 years old

A

Acute lymphoblastic leukemia

295
Q

Symptoms of ALL

A

Nonspecific systemic symptoms (fever, weight loss)

Leukemic cells overcrowd bone marrow- anemia, thrombocytopenia, bone pain

Extramedullary spread- LAD, hepatosplenomegaly, testicular enlargement

mediastinal mass- airway compression and/or superior vena cava syndrome

leptomeningeal spread: neuro symptoms

296
Q

Diagnosis of ALL

A

CBC
Bone marrow biopsy (>20% blasts is diagnostic) with flow cytometry
Lumbar puncture to evaluate for CNS involvement

297
Q

What is the cause of high altitude illness

A

Reduced PiO2 at high altitude (>2500m or 8000ft)

298
Q

Complications of high altitude illness

A

AMS- altered mental status- headache, fatigue nausea

High altitude cerebral edema- increased cerebral blood flow, lethargy, confusion, ataxia

High altitude pulmonary edema- uneven hypoxic vasoconstriction, dyspnea, cough +/- hemoptysis, respiratory distress

299
Q

Treatment for high altitude illness

A

supplemental oxygen

acetazolamide for AMS

dexamethasone for high altitude cerebral edema

descent to lower altitude

300
Q

What is the cause of Zenker diverticulum

A

Impaired UES relaxation (cricopharyngeus muscle) leading to increased intraluminal pressure and herniation causing a PSEUDODIVERTICULUM

301
Q

Clinical manifestations of Zenker diverticulum

A

Age > 60
Men
Insidious, progressive dysphagia
Halitosis, gurgling, crepitus
Regurgitation of undigested food
Aspiration

302
Q

Diagnosis and Treatment of Zenker diverticulum

A

Diagnosis: swallow study with contrast esophagography
Treatment: surgery: cricopharyngeal myotomy and/or diverticulectomy

303
Q

Clinical indicators of clostridium difficile infection progression that warrant surgery

A

Signs of peritonitis: diffuse abdominal tenderness, rebound tenderness
- peritonitis indicates bowel perforation and is a definitive indication for surgical exploration- laparotomy

Colonic dilation: megacolon (colonic diameter >6cm) on abdominal x-ray with associated loss of smooth muscle tone (decreased diarrhea)

Increased serum lactate: possible marker of colonic ischemia

304
Q

Indications for colonic resection (total abdominal colectomy) in c diff colitis patients

A

necrosis
perforation
abdominal compartment syndrome

305
Q

Precipitating factors for hepatic encephalopathy

A

drugs (sedatives, narcotics)
hypovolemia (diarrhea)
electrolyte changes (hypokalemia)
increased nitrogen loan (gi bleeding)
infection (pneumonia, UTI, SBP)
portosystemic shunting (TIPS)

306
Q

Indications for TIPS (transjugular intrahepatic portosystemic shunting)

A

when a patient has ascites that does not respond to medical therapy (diuretics) or has ongoing active or recurrent variceal bleeding even after appropriate treatment with upper endoscopy

307
Q

Clinical signs of idiopathic intracranial hypertension

A

Headache + vision changes
headache quality (positional)
weight changes/elevated BMI
neuro exam

308
Q

What do you do when you suspect increased intracranial pressure

A

do a visual assessment
- visual acuity
- visual fields
- funduscopy

309
Q

If visual assessment shows papilledema what do you do next

A

Evaluate for mass lesions
- urgent imaging (CT/MRI)
- consider venography

310
Q

if mass lesion evaluation is negative then what

A

Lumbar puncture
- if opening pressure >250 and no signs of infection- likely IIH

311
Q

What does a empty sella sign on imaging indicate

A

Increased CSF pressure flattening the pituitary and filling the sella space with fluid

312
Q

What does flattening of the posterior sclera of the eye indicate

A

Transmitted pressure onto the posterior side of the globe which also compresses the optic nerve- the optic nerve sheath is an extension of the arachnoid- leading to papilledema

313
Q

Howell Jolly bodies

A

round dark blue inclusions in red blood cells
- retained RBC nuclear remnants that are typically removed by the spleen
- the presence of them indicates either physical absence of spleen (asplenia) due to congenital absence or surgical removal or functional hyposplenism

314
Q

Twin pregnancy increases risk for what maternal complications

A
  • hyperemesis gravidarum
  • preeclampsia
  • gestational diabetes mellitus
  • iron deficiency anemia
315
Q

Twin pregnancy increases the risk for what fetal complications

A
  • congenital anomalies
  • fetal growth restriction
  • preterm delivery
  • malpresentation
  • monochorionic twins- twin twin transfusion syndrome
  • monoamniotic twins- conjoined twins or cord entanglement
316
Q

What are the causes of decreased central respiratory drive in hypercapnia

A

Drugs (opioids, benzos)
CNS trauma, stroke, encephalitis

317
Q

What are the causes of decreased respiratory neuromuscular function in hypercapnia

A

Spinal cord lesions
ALS
myasthenia gravis

318
Q

What are the causes of decreased thoracic cage or pleural function in hypercapnia

A

Obesity hypoventilation syndrome
Pneumothorax
Rib fractures, flail chest

319
Q

What are the causes of airway obstruction in hypercapnia

A

OSA (upper airway)
COPD (lower airway)

320
Q

What are the causes of impaired gas exchange in hypercapnia

A

Cardiogenic pulmonary edema
Interstitial lung disease

321
Q

Immune etiology of hydrops fetalis

A

RhD alloimmunization

322
Q

Nonimmune causes of hydrops fetalis

A

Parvovirus B19 infection
Fetal aneuploidy
Cardiovascular abnormalities
Thalassemia (hemoglobin Barts)

323
Q

Clinical features of hydrops fetalis

A

pericardial effusion
pleural effusion
ascites
skin edema
placental edema
polyhydramnios

324
Q

How is congenital CMV transmitted

A

bodily fluids (urine, saliva)
- main risk factor- caring for young children

325
Q

Clinical features of congenital CMV

A

growth restriction and microcephaly
periventricular calcifications
hepatosplenomegaly
thrombocytopenia

326
Q

diagnosis and treatment for congenital CMV

A

dx- PCR testing, viral culture of urine/saliva
Treatment- antiviral therapy (valganciclovir) if symptomatic

327
Q

Causes of malignant pericardial effusion

A

Common primary tumors: lung, breast, GI, lymphoma, melanoma

328
Q

Clinical features of malignant pericardial effusion

A

Progressive dyspnea, chest fullness, fatigue
ECG: low QRS voltage and or electrical alternans
CXR: enlarged cardiac silhouette and clear lung fields
ECHO: large effusion and signs of tamponade

329
Q

Treatment for malignant pericardial effusion

A

Acute management: pericardiocentesis, cytologic fluid analysis
Prevention of recurrence: prolonged drainage (catheter, pericardial window)

330
Q

Epidemiology of progressive multifocal leukoencephalopathy

A

JC virus reactivation
Severe immunosuppression (untreated AIDS)

331
Q

How does progressive multifocal leukoencephalopathy present

A

confusion, paresis, ataxia, seizure

332
Q

DX and TX of progressive multifocal leukoencephalopathy

A

Dx- MRI/CT of brain with contrast- shows asymmetric white mater lesions, no enhancement/edema
Lumbar puncture= CSF PCR positive for JC virus
Brain biopsy (rarely needed)

Treatment- often fatal
if HIV + antiretroviral therapy

333
Q

What antihypertensive are associated with reduced insulin sensitivity and increased risk of developing type 2 DM

A

Beta blockers (metaprolol atenolol- beta 1 specific or propnaolol-beta 1 and beta 2)

Beta blockers with combined vasodilatory alpha 1 receptor blocking properties (carvedilol, labetalol) not associated with reduced insulin sensitivity

334
Q

Cushing syndrome signs

A

Cushing syndrome- hypercortisolism
- weight gain
- proximal muscle weakness
- hypertension
- easy bruisability
- dermal atrophy
- wide purple striae
- hyperpigmentation (ACTH dependent Cushing syndrome)
- increased incidence of cutaneous fungal infections (tinea versicolor, onychomycosis)
- hyperandrogenism (menstrual irregularities, acne, hirsutism)

335
Q

Closed spinal dysraphism

A

Failure of posterior vertebral arc fusion
Spinal cord anomalies (lipoma, cyst)
Stretch- induced distal spinal cord dysfunction (tethered cord)

Symptoms- cutaneous or lumbosacral anomalies (hair tuft, mass)
Tethered cord syndrome:
- neurologic: LMN signs
- urologic: incontinence/retention, recurrent UTI
- orthopedic: back pain, scoliosis, foot deformities

Management- MRI of the spine
surgical detethering of cord if symptomatic

336
Q

What causes a focal seizure

A

Neuronal discharge begins in 1 cerebral hemisphere
- symptoms may be motor, sensory or autonomic
- Motor: twitching, sensory: paresthesias, autonomic: sweating
- underlying structural abnormality (tumor)more likely than with a generalized seizure

337
Q

What are the two categories of focal seizures

A

No impairment of awareness
- occurs when seizure remains localized to 1 hemisphere

Impairment of awareness
- occurs when seizure spreads to the other hemisphere
- often associated with automatisms (eg: chewing, picking)

Diagnosis: EEG, Brain MRI

338
Q

What is Todds paralysis

A

Postictal paresis or paralysis

339
Q

Adolescents with myoclonic jerks immediately on wakening

A

Juvenile myoclonic epilepsy

340
Q

By age 5, intellectual disability, severe siezures of varying types (atypical absence, tonic)

A

Lennox Gastaut syndrome
- Interictal EEG demonstrates a slow spike and wave pattern

341
Q

What pathogens are airborne and what are isolation precautions for airborne pathogens

A

Bacterial: tuberculosis
Viral: primary VZV (chickenpox), disseminated VZV reactivation (shingleszoster) in immunocompromised patients, COVID19, measles

Requirements: negative pressure room, N95 respirator

342
Q

What pathogens are contact spread and what are isolation precautions for contact pathogens

A

MRSA, VRE, Extended spectrum beta lactamase producing (ESBL producing
Bacterial: C.diff, E.coli 0157:H7
Viral: RSV, primary VZV (chickenpox), disseminated VZV reactivation (shingles/zoster), dermatomal ZVZ reactivation (shingles/zoster)

Requirements: gowns and gloves, single-use equipment (stethoscope)

343
Q

What pathogens are spread by droplets and what precautions are needed

A

Bacterial: Neisseria meningitides, Hflu Type B, Mycoplasma pneumoniae

Viral: influenza virus, adenovirus

Requirements: mask within 3-6ft of patient

344
Q

What are the clinical features of paroxysmal nocturnal hemoglobinuria

A

Hemolysis -> fatigue
Cytopenias -> impaired hematopoiesis
Venous thrombosis -> intraabdominal, cerebral veins

345
Q

Workup for paroxysmal nocturnal hemoglobinuria

A

CBC (hypoplastic/aplastic anemia, thrombocytopenia, leukopenia)

elevated LDH and low haptoglobin (signs of hemolysis)

indirect hyperbilirubinemia

urinalysis (hemoglobinuria)

flow cytometry (absence of CD55 and CD59)

346
Q

Treatment for paroxysmal nocturnal hemoglobinuria

A

Iron and folate supplementation

Eculizumab (monoclonal antibody that inhibits complement activation)

347
Q

Causes of chronic pancreatitis

A

Alcohol use
Cystic fibrosis (common in children)
Ductal obstruction (malignancy, stones)
Autoimmune

348
Q

Clinical presentation of chronic pancreatitis

A

Chronic epigastric pain with intermittent pain-free intervals

Malabsorption: steatorrhea, weight loss

Diabetes mellitus

349
Q

Laboratory results/imaging of chronic pancreatitis

A

Amylase/lipase can be normal and nondiagnostic

CT scan or MRCP can show calcifications, dilated ducts and enlarged pancreas

350
Q

Treatment of chronic pancreatitis

A

Pain management
Alcohol and smoking cessation
Frequent small meals
Pancreatic enzyme supplements

351
Q

What does fecal elastase check for

A

In patients with chronic pancreatitis= destruction of pancreatic islet and acinar cells leads to endocrine and exocrine insufficiency resulting in protein and fat malabsorption, steatorrhea, weight loss, fat soluble vitamin deficiencies

Fecal elastase- noninvasive test for severe pancreatic exocrine insufficiency
- alternate noninvasive test s is serum trypsinogen

352
Q

What markers are seen in inflammatory bowel disease

A

Increase in both fecal calprotectin and fecal leukocytes

352
Q

What markers are seen in celiac disease

A

Celiac disease presents as steatorrhea and weight loss which can result from malabsorption
- typically celiac disease patients have IDA and other autoimmune comorbidities

Tissue transglutaminase antibodies are elevated in celiac disease

353
Q

Hard signs of traumatic arterial injury

A

Require immediate surgery

Distal limb ischemia (paralysis, pain, pallor, poikilothermy)

Absent distal pulse

Active hemorrhage or rapidly expanding hematoma

Bruit or thrill at site of injury

354
Q

Soft signs of traumatic arterial injury

A

Require further imaging

Diminished distal pulses

Unexplained hypotension

Stable hematoma

Documented hemorrhage at time of injury

Associated neurologic deficit

355
Q

What is the diagnostic modality of choice for traumatic arterial injury

A

CT angiography - high sensitivity and specificity and rapid procedure time

356
Q

Uncomplicated fractures of the middle third of the clavicle- how are they treated

A

Nonoperatively with rest, ice and either a sling or a figure of eight bandage

357
Q

Fractures of the distal third of the clavicle are treated how?

A

open reduction and internal fixation to prevent nonunion

358
Q

Diamon Blackfan anemia

A
  • congenital erythroid aplasia
  • craniofacial abnormalities
  • TRIGPHALANGEAL THUMBS
  • increased risk of malignancy
  • macrocytic anemia
  • reticulocytopenia
  • normal platelets, white blood cells

TREATMENT- corticosteroids, RBC transfusions

359
Q

How does Diamond Blackfan anemia present in infancy

A

Progressive pallor and poor feeding due to anemia

Heart rate increases to meet oxygen demands and a faint systolic ejection murmur due to increased turbulence across the valves

360
Q

Fanconi anemia signs

A

Pathogenic variants in genes involved in DNA repair
- pancytopenia- FA leads to low levels of RBCs, WBCs and platelets (WHILE DIAMOND BLACKFAN IS SELECTIVE DECREASE IN RBC FORMATION)

361
Q

Asymptomatic Hypercalcemia

A
  • normal renal function
  • high-normal PTH level
  • low urinary calcium excretion

FAMILIAL HYPOCALCIURIC HYPERCALCEMIA
- benign autosomal dominant disorder caused by a mutation of the calcium sensing receptor
- normally high calcium levels suppress PTH secretion by parathyroid glands
- in FHH higher calcium concentrations are required to suppress PTH release
- defective CaSR leads to increased reabsorption of calcium in renal tubules

362
Q

Primary hyperparathyroidism vs Familial hypocalciuric hypercalcemia

A

Primary hyperPTH- increased urinary calcium excretion due to excessive mobilization of calcium from bones
UCCR >0.02

FHH- low urinary calcium levels (<100mg24hr)
UCCR <0.01

363
Q

Side effects of calcineurin inhibitors (tacrolimus, cyclosporine)

A
  • inhibit the transcription of Il2 to reduce T lymphocyte activity and are important component of chronic immunosuppression following solid organ transplantation

Side effects:
- nephrotoxicity: can lead to reversible AKI or slow progressive chronic kidney injury that is irreversible
- hyperkalemia, hyperuricemia with increased rates of gout
- HTN
- neurotoxicity- tremor, visual disturbance, seizures
- glucose intolerance
- gingival hypertrophy, hirsutism, alopecia
- GI disturbance

364
Q

Vaginal cancer- risk factors, features, diagnosis and treatment

A

Risk factors- age >60, HPV infection, tobacco use, in utero DES exposure (clear cell adenocarcinoma only)

Clinical features- vaginal bleeding, malodorous vaginal discharge, irregular vaginal lesion

Diagnosis- vaginal biopsy

Management- surgery +/- chemoradiation

365
Q

Neurofibromatosis Type 1- chromosome 17

A

Cafe au lait macules
Scoliosis
Axillary and inguinal freckling
Neurofibromas
Pseudoarthrosis
Optic glioma
Lisch nodules
Increased risk of neurologic disorders (cognitive deficits, learning disabilities, seizures and intracranial neoplasms)

AUTOSOMAL DOMINANT NEUROCUTNEOUS DISORDER

366
Q

Neurofibromatosis Type 2- chromosome 22

A

Acoustic neuromas (vestibular schwannomas)
Do not have cafe au lait macules or axillary or inguinal freckling

367
Q

Tuberous Sclerosis

A

Ash lead spots
Angiofibromas
Shagreen patches
Seizures (infantile spasms)
Developmental delay
Behavior problems- hyperactivity, self injury
White patches on the retina
Intracardiac rhabdomyomas

368
Q

Fragile X syndrome

A

Testicular enlargement in the setting of seizures
X-linked disorder
Intellectual disability
Large ears
Long and narrow face
Macroorchidism

369
Q

Sturge Weber Syndrome

A

Port wine stain on the face
Ocular disease (visual deficits or glaucoma)
leptomeningeal capillary-venous malformations- increased risk for seizures

370
Q

Unilateral vs bilateral vestibular schwannoma

A

Unilateral- vestibular schwannoma
Bilateral- NF Type 2

371
Q

Cholesteatoma

A

Erosive, expansile mass of keratin debris in the middle ear

Presents with unilateral conductive hearing loss (bone conduction > air conduction, lateralization to the affected ear)

Otorrhea

Pearly white mass in the middle ear

372
Q

Legg Calve Perthes Disease

A
  • avascular necrosis (fragmented, collapsed epiphysis)
  • commonly affects boys age 5-7 and presents with insidious onset of hip pain and limp
  • X ray may be normal in early disease or show fragmentation of the femoral head
373
Q

SCFE

A
  • anteriolateral and superior displacement of the proximal femur along the physis
  • during periods of accelerated growth (growth spurts in tall thin children) or obesity
  • classic presentation- insidious onset of dull hip pain and limp
  • minor trauma can exacerbate symptoms
  • patients hold affected hip in passive external rotation and exhibit decreased internal rotation, abduction and flexion
  • hip radiographs- diagnostic
  • treatment- immediate stabilization of the physis with surgical fixation
374
Q

TTP

A
  • low ADAMTS13 level- leads to platelet trapping and activation
  • hemolytic anemia (high LDH, low haptoglobin) with schistocytes
  • thrombocytopenia (high bleeding time, normal PT/PTT)
  • sometimes with renal failure, neuro manifestations, fever

Tx- plasma exchange, glucocorticoids, rituximab, caplacizumab

375
Q

Incisional Hernia

A
  • breakdown of prior fascial closure
  • commonly seen in obesity, tobacco smokers, poor wound healing, vertical or midline incision, surgical site infection

features: abdominal mass that enlarges with valsalva
- palpable fascial edges in nonobese patients
- possible delayed presentation

dx- clinical, CT abdomen

376
Q

Androgen insensitivity Syndrome

A

X linked mutation in androgen receptor
Genotypically male (46 XY)
Phenotypically female
Breast development
Absent or minimal axillary and pubic hair
Female external genitalia
Absent uterus, cervix, and upper one third of vagina
Cryptorchid testes

Management- gender identity/assignment counseling and gonadectomy (malignancy prevention)

377
Q

Primary Adrenal insufficiency

A

destruction of bilateral adrenal cortex
- caused by autoimmune adrenalitis or infection or malignancy

Low cortisol
low aldosterone
high ACTH

Hypovolemia
Hyperkalemia
Hyponatremia
Hyperpigmentation

378
Q

Secondary adrenal insufficiency

A

Disruption of hypothalamic pituitary axis

Due to chronic glucocorticoid therapy, infiltrative disease or ischemia of anterior pituitary gland

Low cortisol
NORMAL aldosterone
low ACTH

euvolemia
minimal electrolyte disturbance
no hyperpigmentation
less severe symptoms

379
Q

Migratory superficial thrombophlebitis (aka Trousseau syndrome)

A

Chronic disseminated intravascular coagulopathy

Recurrent superficial venous thrombosis at unusual sites (arm, chest)

STRONGLY associated with occult visceral adenocarcinoma (pancreas, lung)

complications include venous thrombosis, verrucous endocarditis, ischemic stroke, arterial emboli

DX- CT of the abdomen if epigastric pain despite antacid therapy

TX- heparin therapy to prevent future clots

380
Q

Metatarsus adductus

A

Medial deviation of the forefoot
- neutral position of hindfoot
- flexible positioning typical

Tx- reassurance

381
Q

Clubfoot

A
  • medial/upward deviation of forefoot and hindfoot
  • hyperplantar flexion of the foot
  • rigid position typical (congenital clubfoot)

Tx- serial manipulation and casting; surgery for refractory cases

382
Q

Acute postoperative mediastinitis

A

Direct microbial contamination of operative sites which complicates 1-2% of cardiothoracic operations involving sternotomy

presents 1-2 weeks after operation as sepsis (fever, tachy, leukocytosis), signs of sternal wound infection (drainage and tenderness) and chest x ray showing localized mediastinal fluid or air

dx- characteristic clinical presentation and surgical exploration revealing pus in mediastinum

tx- IV abx and surgical debridement

383
Q

Miliary tuberculosis

A

fever, cough, lethargy and respiratory failure with numerous micronodular lesions in the liver, lungs, and spleen

caused by lymphohematogenous spread of Mycobacterium tuberculosis
- rare but serious complication of primary TB in hosts with poor T cell function (infants and immunocompromised)

384
Q

Risk factors for cerebral palsy

A

Prematurity
low birth weight
intrauterine infection
perinatal complications (placental abruption, hypoxic-ischemic injury, stroke)

385
Q

Clinical features of cerebral palsy

A

Spastic
- affects 1 or more limbs
- hypertonia
- motor delay
- commando crawling- diplegia
- early hand preference
- contractures

Dyskinetic (choreoathetotic, dystonic): involuntary movements, dysarthria

Ataxia: hypotonic, incoordination, jerky speech

386
Q

Acute left renal vein thrombosis

A

Membranous neprhopathy is a common cause of nephrotic syndrome

  • occlusion of L renal vein increases glomerular pressure and causes hematuria and L sided flank pain
  • L gonadal vein drains into the L renal vein, obstruction also causes L gonadal vein dilation
  • Risk factors for RVT- nephrotic syndrome, renal malignancy and trauma
387
Q

Brown recluse spider bite

A

Common when people are putting their clothes on

  • small ulcer developing at site of a recent bite
  • many cases result in a small papule that heals in days to weeks
  • in some cases, a deep skin ulcer develops at the bite site over the course of a few days with an erythematous halo and a necrotic center than can progress to an eschar
388
Q

Black widow spider bites

A

Lead to more pronounced local and systemic manifestations due to the effects of the toxin
- muscle pain, abdominal rigidity, and muscle cramps
- ulceration is uncommon
- patients commonly develop nausea and vomiting within hours of the bite

389
Q

Snake bites

A

hemoglobinuria, bleeding, muscle paralysis
severe local pain, swelling, and discoloration within hours of the bite

390
Q

Treatment of preeclampsia with severe features

A

Severe features- hypertension, headache, visual changes
- in patients without MG, treat with magnesium sulfate sor seizure prophylaxis
- in patients with MG, magnesium sulfate is CONTRAINDICATED because it may trigger a myasthenic crisis (oropharyngeal muscle weakness, respiratory failure requiring intubation) due to inhibition of acetylcholine release at the NMJ
- IN THESE PATIENTS SEIZURE PROPHYLAXIS IS WITH VALPROIC ACID

391
Q
A

UWORLD REVIEW (2 decks)

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