Interne Flashcards

1
Q

which changes in eletrolyten kun je verwachten bij tumor lysis syndrome ?

A
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2
Q

when does tumor lysis syndrome start?

A

most commonly occurs after initiating cytotoxic treatment; breakdown of cancer cells

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3
Q
A

a

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4
Q

febrile neutropenia, what to do?

A

epiric AB should bre started within the first hours of onset, like meropenem (better than ceftriaxon or cefuroxime or vanco), those who continue to have persistent fever of unidentified cause following 4 to 7 days of ab, should be given epiric antifungal therapy like amphotericin B

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5
Q
A

d

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6
Q
A

c

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7
Q
A

b

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8
Q
A

b

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9
Q

pernicious anemia?

A
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10
Q

causes B12 defi

A
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11
Q

difference between anemia due to folate def or vitamin b12 def?

A

Vitamin B12 deficiency causes neurological symptoms due to demyelination of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts (subacute combined degeneration).
Folate deficiency does NOT cause neurological symptoms.
Methylmalonic acid (MMA) is elevated in vitamin B12 deficiency but normal in folate deficiency.
Both cause elevated homocysteine levels.

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12
Q

Starting folate treatment before excluding vitamin B12 deficiency may correct anemia, but it can worsen neuropathy!

A

TRUE

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13
Q

hypersegmented neturophils seen in

A

b12 def anemia

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14
Q
A
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15
Q
A
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16
Q

iemand from the middle east + jaundice + high reticulocyte

A

avoid aspirin

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17
Q

ieman from the middel eat + recurrent fever + arthralgia or and abdomianal pain, chest pain

A

avoid amoxicillin, macrolide, steroid, verapamil/diltiazem

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18
Q

The incubation period of malaria is a minimum of seven days (7-30 days); if fever occurs before the seventh day following exposure in an endemic region, it is most likely

A

not due to malaria

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19
Q

malaria common symptoms

A
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20
Q

malaria epidemioogy

A
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21
Q

malaria prophylaxis

A

you should give atorvaquone-proguanll

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22
Q

atorvaquone-proguanll alternative if someone has psychiatrisch vg

A

doxycycline

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23
Q

treatmetn of malaria

A
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24
Q

malaria medicatie met veel resistence

A

chloroquine

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25
Q

plasmodium falciparum blood smear

A

ring

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26
Q

the primary vector of dengue fever is aedes aegypli mosquito, the peak period for the infection

A

early morning

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27
Q

iemand met retro orbitaal pain met spierlijn en joint pains met koorts

A

denk aan dengue fever Duration of febrile phase of dengue fever: usually 2–7 days; If symptoms appear more than 2 weeks after returning from a dengue-endemic region, it is very unlikely that dengue is the cause.

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28
Q

dd bij dengue fever

A

malaria, zika virus en chikungunya fever; Severe hemorrhagic manifestations with shock and death as well as decreased neutrophil and platelet counts are more indicative of Dengue fever than Chikungunya fever.

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29
Q

fever in travelers southeast asia

A

dengue fever

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30
Q

fever in travelers from sub saharan afrikca

A

malaria

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31
Q

when the malaria test is negeat

A

repeat it every 6-12 hours for 48 hours

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32
Q

how to supplement iron in patient with gastritis

A

must be iv iron not po

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33
Q

transfusion reactions

A
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34
Q

when can you give iron supplement to a baby

A

at 4 months of age or older but not earlier because they would have enough reserves

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35
Q

causes of hemochromatosis

A

primary door genetica, secondary door transfusie danwel thalassemia danwell sickle cell anemia

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36
Q

treatment of hemochromatosis

A

regular therapeutic phlebotomy

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37
Q

diagnostiek hemochromatosis

A
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38
Q

hemochromatosis epidemiologie

A
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39
Q

meest bekende leukemia in kids

A

all, followed by aml, and leukemia is the most common cancer in children

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40
Q

hemato maligniteit bij ouderen

A

cll

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41
Q

iemand komt bij jouw poli met polymyalgia rheumatic, welke hemato malginiteit geassocaieert met deze

A

CLL

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42
Q

There should be suspicion for ……… in a child with thrombocytopenia and petechiae following a viral illness!

A

ITP ; Splenomegaly is very unusual in ITP and makes other diagnoses more likely!

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43
Q
A

C

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44
Q
A

c

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45
Q

treatment of ITP

A
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46
Q

splenectomy is a treatment of

A

itp, want het milt is de locatie van de destructie van bloedplaatejs

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47
Q

clinical features of TTP.

A

“Nasty Fever Ruined My Tubes:” Neurological symptoms, Fever, Renal function impairment, Microangiopathic hemolytic anemia, Thrombocytopenia are the clinical features of TTP.
The typical patient is a previously healthy adult presenting with mental status changes, fever, petechiae, fatigue, and pallor. Laboratory tests will then indicate hemolytic anemia and possibly acute kidney injury (AKI). Impaired kidney function may not be present, and only a minority of patients will present with all five clinical findings.
median age at diagnosis: ∼ 40 years
More common in women

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48
Q

lab of TTP

A

While PT and aPTT are normal or only mildly elevated in TTP and HUS (no consumption coagulopathy), they are markedly elevated in disseminated intravascular coagulation (consumption of platelets and all coagulation factors

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49
Q

A normal adult has three main types of hemoglobin:

A
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50
Q

which variants do you have in beta thalassemia?

A
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51
Q

Why These Changes Happen?
why happens in beta thalasemia

A
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52
Q

what distinguishes iron deficiency anemia from beta thalassemia?

A
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53
Q

afwijkingen related to alpha thalassemia

A
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54
Q
A
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55
Q

explain sickle cell disease and you know about it

A
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56
Q

sickle cell trait vs disease

A
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57
Q

what are the acute manifestations that you can expect to see in a patient with sickle cell disease?

A
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58
Q
A

a

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59
Q

initial managment sickle cell disease

A

iv fluid and analgesia

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60
Q

Exchange transfusions vs simple in sickle cell disease?

A
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61
Q
A

a

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62
Q
A

c

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63
Q

what do you know about Splenic sequestration in sickle cell disease?

A

ong-term management
Patients/caregivers should be taught to monitor spleen size to detect recurrence early.
Splenectomy or partial splenectomy may be indicated (e.g., for hypersplenism or life-threatening or recurrent sequestration events) [1]

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64
Q
A

c

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65
Q
A

a

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66
Q

what do you know about aplastic crisis in sickle cell disease

A
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67
Q
A

a

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68
Q

Possible etiologies of acute anemia in sickle cell disease include

A

aplastic crisis, splenic sequestration, acute hepatic sequestration, acute chest syndrome, delayed hemolytic transfusion reaction, infection, sepsis, and acute blood loss (not necessarily linked to sickle cell disease)

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69
Q

sickle cell anemia microscopie

A

Peripheral blood smear findings may include:
Crescent-shaped sickled RBCs (drepanocytes or sickle cells)
Target cells
Howell-Jolly bodies: occur with splenic dysfunction

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70
Q
A

memorize

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71
Q

The mnemonic “STOP Making Trouble!” helps to recall the etiology of

A

DIC: S – Sepsis/Snakebites, T – Trauma (acute traumatic coagulopathy), O – Obstetric complications, P – Pancreatitis, M – Malignancy, T – Transfusion.

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72
Q

diagnosis dic

A
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73
Q

dic info

A
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74
Q

dic treatment

A
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75
Q

good to know

A
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76
Q

classic triad of hereditary spherocytosis

A

usually presents in infancy or childhood with the classic triad of anemia, jaundice, and splenomegaly.; soms black pigment gallstones that lead to cholecystitis
it is autosomal dominant; positive familie anamnese for splenectomy and or developed cholelithiasis at young age

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77
Q

hereditary spherocytosis lab findings (mention 7)

A
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78
Q

definitive treatment

A

splenectomy

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79
Q
A
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80
Q
A

hereditary spherocytosis

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81
Q

thrombotic thrombocytopenic purpura epidemiologie

A
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82
Q

thrombotic thrombocytopenic purpura presentation

A

The typical patient is a previously healthy adult presenting with mental status changes, fever, petechiae, fatigue, and pallor. Laboratory tests will then indicate hemolytic anemia and possibly acute kidney injury (AKI). Impaired kidney function may not be present, and only a minority of patients will present with all five clinical findings.

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83
Q
A

c

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84
Q

thrombotic thrombocytopenic purpura lab

85
Q

ttp vs itp?

86
Q

The typical HUS patient is

A

a preschooler who has had a diarrheal illness within the past 5–14 days and presents with petechiae, jaundice, and oliguria.

88
Q
A

B. squamous cell carcinoma has strong association with smoking, adenocarcinoma most common type of primary lung cancer and more common in women and nonsmokers

90
Q

what to do for lung nodules ?

91
Q
A

c; squamous cell carcinoma is associated with hypercalcemia

92
Q

if you see fingernail clubbing

A

denk aan bronchogenic carcinoma, please note that copd does not cause clubbing but if clubbing is present in copd, you need to rule out maligniteit

93
Q

superior vena cava syndroom

A

associated with cancer in the apical of the lung like pancoast tumor or non small cell carcinoma , with also horner syndroom

99
Q

best way for smoking cessation in pregnancy

A

behavioral therapy

100
Q

second best way for smoking cessation in pregnancy

A

nictoine replacement therapy

107
Q

which is the most effective preventivce measrue to improve post myocardial infarction prognosis? lowering lipid or smoking cessation?

A

stopping smoking

110
Q
112
Q

community aquired pneumonia oorzaak

A

most common is streptoococcus pneumoniae, also is the most common in nursing home, also in drugs users, ook vaak labor pneumoni

andere oorzaken staphylococcus aureas, klebsiella pneumonia, H. infueza;; all of these typical pneumonia

andere oorzaken voor atypische pneumonie: mycoplasma pneumonie, chlamydia pneumonie, legionella, coxiella burnetie, en viruses zoals rsv, cmv, adenovirus, influenza en parainfluenza

113
Q

hosptial aquired pneumonia;;

A

gram negative pathogens like psudomonas, entre baacteriacae, streptococcus pneumonia, staphylococcus auras

114
Q

criteria for admission for pneumonia

117
Q

Empiric antibiotic therapy for community-acquired pneumonia in an outpatient setting

119
Q

Empiric antibiotic therapy for community-acquired pneumonia in an inpatient setting

120
Q
A

a; this is also true for those admitted to the icu

125
Q
A

b, the key for the question is cold agglutination which is a remark for atypical pneumonia

126
Q
A

a
andere oorzaken in kinderen: Streptococcus pneumoniae
Chlamydia trachomatis (in infants)
Chlamydia pneumoniae (in young children and adolescents)
Mycoplasma pneumoniae , en ook RSV

127
Q
A

patchy opacities bilaterally that allies well with mycoplasma pneumonia

128
Q

bronchogenic cancer with multiple thoracentesis , what shoudl be added tot the management

A

thoractomy; malignant pleural effusion is a very disabling condition, you need thoractomy because it is maligneant

135
Q

define copd, chronic bronchiitis and emphysema

136
Q

best diagnostics for emphysema

137
Q

Interpretation of DLCO

A

dlco in chroic bronchitis can be normal or high but in emphysema is low

139
Q

what happens to lung compliance in copd

140
Q

what does increase and improve surival in copd patients with cor pulmonary

A

long term o2 therapy, when considering only copd, then smoking cessation

141
Q

how to follow up copd

A

fev1, and that is good for disease progression and prognosis

142
Q

what does improve survival in advanced copd aptients

143
Q

in which patients you can get false positive bnp

144
Q

copd exacerbation with a mouth full of secretions

A

invasive mechanical ventilation

145
Q

copd patient not responding to salbutamol

A

next is ipratrpium

146
Q

home oxygen in copd, when?

A

and the best to delive oxygen is via venturi bag oxygen

147
Q

how to treat spntaneous pneumothorax in copd

A

chest tube

156
Q

hepatitis after restuarant visit; or young pt with yellow sclera

A

it is hepatitis A

157
Q

explain the clinical presentation of gilbert syndrom; age of onset, etiology, inheritance, clinical features, triggers, diagnosis

158
Q

explain the clinical presentation of crigler najjar; age of onset, etiology, inheritance, clinical features, triggers, diagnosis

160
Q
A

c; vanwege het risico op maligniteit

163
Q

hepatitis c treatment

164
Q

hepatitis b treatment

166
Q

risk hcv transmission by needle stick injury

167
Q

hcv most common genotype in SA

169
Q
A

chronic hepatitis B

171
Q

what do you know about serology and hepatitis B

173
Q

mention what you know about serology in hebatitis b

174
Q

the first marker of actue infection in hepatitis b is

179
Q

mention the serology of 4 sceniario’s

180
Q
A

the patient has positive hcv antibody test, indicating exposure to hcv at some point, however the negative hcv rna testing suggests that there is no ongoing active infection

183
Q

hemochromatosis lab

184
Q

primary biliary cirrhosis

A

Primary biliary cholangitis (PBC; also known as primary biliary cirrhosis) is a chronic progressive liver disease of autoimmune origin that is characterized by destruction of the intralobular bile ducts. The pathogenesis of PBC is unclear. PBC is frequently associated with other autoimmune conditions and primarily affects middle-aged women. In the early stages, PBC is typically asymptomatic. Fatigue is the most common initial symptom. In advanced disease, increased fibrotic changes lead to typical signs of cholestasis (e.g., jaundice), portal hypertension (e.g., ascites, gastrointestinal bleeding), and severe hypercholesterolemia (e.g., xanthomas, xanthelasmas). Elevated alkaline phosphatase (ALP) levels, antimitochondrial antibodies (AMA), and liver biopsy findings can establish the diagnosis. Management involves supportive care, e.g., management of cholestasis-associated pruritus, and slowing disease progression with ursodeoxycholic acid. Liver transplantation is the only definitive treatment.

185
Q

autoimmune hepatitis

A

Autoimmune hepatitis (AIH) is a rare form of chronic hepatitis that predominantly affects women. Although the etiology is unclear, it is commonly associated with other autoimmune conditions (e.g., thyroid disease, type 1 diabetes mellitus, celiac disease). The clinical presentation ranges from asymptomatic transaminitis to acute liver failure. Diagnosis is established based on the detection of autoantibodies (e.g., antinuclear antibodies, anti-smooth muscle antibodies) and the histologic findings of interface hepatitis on liver biopsy. Treatment consists of immunosuppressive medications such as prednisone and azathioprine. The prognosis is favorable with treatment; without treatment, patients may develop cirrhosis and liver failure.

186
Q

(Nonalcoholic fatty liver disease, NAFLD) treatment

A

reduce weight, lifestyle, like for af

187
Q
A

d; what are the lab findings

189
Q

multiple hypo dense lesions in the liver

A

denk aan hepatocellular carcinoma

190
Q

hepatocellualr carcinoma treatment

193
Q
A

ultrasound is the best initial exam, then if you find nodule do triphasic ct

195
Q
198
Q
A

mensen met overvulling, behandel de overvulling eerst

202
Q

what do you know about splenic vein thrombosis

204
Q

what should you avoid if you have hepatic hemangioma?

A

excessive sport or contact sport and trauma, and if the women using OCP, then she should stop with it

205
Q

describe the hemangioma in MRI

208
Q
A

b; the managment is reassure